Atividades Biolgicas de Compostos Vegetais

Journal of Ethnopharmacology 263 (2020) 112792
Contents lists available at ScienceDirect
Journal of Ethnopharmacology
journal homepage: www.elsevier.com/locate/jethpharm
Traditional uses, chemical diversity and biological activities of Panax L. T

(Araliaceae): A review
Lu Liua,b, Fu-Rong Xub,∗∗, Yuan-Zhong Wanga,∗
a
Medicinal Plants Research Institute, Yunnan Academy of Agricultural Sciences, Kunming, China
b
College of Traditional Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, China
ARTICLE INFO ABSTRACT:
Keywords: Ethnopharmacological relevance: Panax L. (Araliaceae) is globally-recognized plant resource suitable for the
Panax L. (Araliaceae) globalization of traditional Chinese medicines. It has traditionally been used as tonic agents in various ethno
Botanical natural products medicinal systems of East Asia, especially in China. It is often used to regulate bodily functions and considered as
Chemical diversity adjuvant therapy for tumor, resuscitation of traumatic hemorrhagic shock, etc.
Biological activities
Aim of this review: This review systematically summarized the information on distributions, botanical char
Review
acteristics, traditional uses, chemical components and biological activities of the genus Panax, in order to explore
and exploit the therapeutic potential of this plant.
Materials and methods: The available information about genus Panax was collected via the online search on Web
of Science, Google Scholar, PubMed, Baidu Scholar, Science Direct, China National Knowledge Infrastructure
and Springer search. The keywords used include Panax, saponin, secondary metabolites, chemical components,
biological activity, pharmacology, traditional medicinal uses, safety and other related words. The Plant List
(www.theplantlist.org) and Catalogue of Life: 2019 Annual Checklist (www.catalogueoflife.org/col/) databases
were used to provide the scientific names, subspecies classification and distribution information of Panax.
Results: Panax is widely assessed concerning its phytochemistry and biological activities. To date, at least 748
chemical compounds from genus Panax were isolated, including saponins, flavonoids, polysaccharides, steroids
and phenols. Among them, triterpenoid saponins and polysaccharides were the representative active ingredients
of Panax plants, which have been widely investigated. Modern pharmacological studies showed that these
compounds exhibited a wide range of biological activities in vitro and in vivo including antineoplastic, anti-
inflammatory, hepatorenal protective, neuroprotective, immunoregulatory, cardioprotective and antidiabetic
activities. Many studies also confirmed that the mechanisms of organ-protective were closely related to mole
cular signaling pathways, the expression of related proteins and antioxidant reactions. To sum up, genus Panax
has high medicinal and social value, deserving further investigation.
Conclusions: The genus Panax is very promising to be fully utilized in the development of nutraceutical and
pharmaceutical products. However, there is a lack of in-depth studies on ethnomedicinal uses of Panax plants. In
addition, further studies of single chemical component should be performed based on the diversity of chemical
structure, significant biological activities and clinical application. If the bioactive molecules and multi
component interactions are discovered, it will be of great significance to the clinical application of Panax plants.
It is an urgent requirement to carry out detailed phytochemical, pharmacology and clinical research on Panax
classical prescriptions for the establishment of modern medication guidelines. Exploring the molecular basis of
herbal synergistic actions may provide a new understanding of the complex disease mechanisms and accelerate
the process of pharmaceutical development.
1. Introduction have been constantly made to explore reliable alternative therapies and
the medicinal natural products, especially those derived from plants
With the enhancement of public health awareness, great efforts due to the appearance of toxic side of chemical drugs and
∗
Corresponding author.
∗∗
Corresponding author.
E-mail addresses: [email protected] (F.-R. Xu), [email protected] (Y.-Z. Wang).
https://doi.org/10.1016/j.jep.2020.112792
Received 5 November 2019; Received in revised form 22 March 2020; Accepted 22 March 2020
Available online 18 April 2020
0378-8741/ © 2020 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license
(http://creativecommons.org/licenses/by/4.0/).
L. Liu, et al. Journal of Ethnopharmacology 263 (2020) 112792
Table 1
Name and distribution of genus Panax plants.
Scientific name Rank Common name Distribution Area
Panax assamicus R.N.Banerjee Species – Assam and East Himalaya

Panax bipinnatifidus Seem. Species “Yuye San-chi” Assam, China North-Central, China South-Central, East Himalaya; Myanmar,
Nepal, Thailand, Tibet and West Himalaya
Panax bipinnatifidus var. angustifolius (Burk.) Infraspecific taxon – Assam, China South-Central, East Himalaya, Nepal, Thailand, Tibet and West
J. Wen Himalaya
Panax bipinnatifidus var. bipinnatifidus Infraspecific taxon – China North-Central, South-Central, East Himalaya, Myanmar, Nepal and
Thailand
Panax ginseng C. A. Mey. Species Korean ginseng, Ginseng China North-Central, Khabarovsk, Korea, Manchuria and Primorye
Panax japonicus (T. Nees) C. A. Mey. Species Japanese ginseng or “Zhu- From the southern foot of the Himalayas to the east, through southern China to
Jie-Shen” the Japanese islands, the western end of Nepal, Bhutan and the hinterland of
the Himalayas
Panax notoginseng (Burk.) F. H. Chen Species Chinese ginseng, “San-chi” South Yunnan, Alpine Mountains in Western Sichuan, China South-Central and
Southeast
Panax pseudoginseng Wall. Species Himalayan ginseng The narrow mountains of southern Tibet, China and Nepal in the middle of the
Himalayas
Panax quinquefolium L. Species American ginseng From Quebec in eastern Canada to Mambatoba in the West and then south to
Florida, Alabama and Oklahoma in the United States
Panax sokpayensis Shiva K. Sharma & Pandit Species – East Himalaya
Panax stipuleanatus H. T. Tsai & K. M. Feng Species “Wild-San-chi”, “Xiang-ci” From southern Yunnan to tropical monsoon rain forest in northern Vietnam
and “slub San-chi”
Panax trifolius L. Species Dwarf ginseng Connecticut, Delaware, Georgia, Indiana, Kentucky, Maine, Maryland,
Masachusettes, Michigan, Minnesota, New Brunswick, New Hampshire, New
Jersey, New York, North Carolina, Nova Scotia, Ohio, Ontario, Pennsylvania,
Prince Edward I., Quebec, Rhode I., Tennessee, Vermont, Virginia, West
Virginia and Wisconsin
Panax vietnamensis Ha & Grusha. Species Vietnamese ginseng China North-Central, China South-Central, China Southeast and Vietnam
Panax vietnamensis var. fuscidiscus K. Infraspecific taxon Vietnamese ginseng China South-Central
Komatsu, S. Zhu & S. Q. Cai
Panax vietnamensis var. langbianensis N. V. Infraspecific taxon Vietnamese ginseng Vietnam
Duy, V. T. Tran & L. N. Trieu
Panax vietnamensis var. vietnamensis Infraspecific taxon Vietnamese ginseng China North-Central, China South-Central, China Southeast and Vietnam
Panax wangianus S. C. Sun Species – China South-Central
Panax zingiberensis C. Y. Wu & K. M. Feng Species Ginger ginseng From southern Yunnan to Tropical monsoon rain forest in northern Vietnam
—: not mentioned.
uncontrollable risks of biological agents. Botanical (plant-based) nat medicinal treatise, recorded that P. ginseng leaves had the effect of
ural product is defined as the substance produced by a variety of natural “replenishing qi, invigorating lung, expelling the heat and promoting
sources which can be either a complex mixture extracted from raw the production of the body fluid”. Flowers of P. ginseng played a role of
material or a single-compound (Kellogg et al., 2019). In this regard, aromatic resuscitation (Zhao, 1998). In other medical monographs,
some medicinal plants, such as genus Panax plants, have been well “Ben Jing Feng Yuan” (in Chinese) demonstrated that the rhizomes of
acknowledged to show great advantages over other chemical drugs. P. ginseng could induce vomiting, however, which was denied by
Panax was derived from the Greek word meaning “all-healing” and modern studies. In addition, fibrils of P. ginseng were also reported to be
primarily coined by the Russian botanist Carl A. Meyer. Genus Panax capable of effectively treating vomiting, cough and blood loss, as well
belongs to the Araliaceae family (Commission, 2015). Currently, a total as other syndromes (Zhang, 1996). Although different species and parts
of 18 plant species including infraspecific taxa, have been proved to be of Panax plants have diverse usages in the Traditional Chinese medi
members of the Panax globally, which can be found in Table 1 (Yahara cines (TCMs) system, most of them was considered saponins as the main
et al., 1978). The representative members of the Panax include P. gin active ingredients (Bai et al., 2014). So far, the main chemical com
seng C.A. Mey, P. quinquefolius L., P. notoginseng (Burk.) F.H. Chen, etc pounds have been isolated from the genus Panax include saponins,
(Yang and Fang, 1991). Originated from “East Asia-North America” in flavonoids, polysaccharides, phytosterols, polyacetylenes, amino acids
paleotropical mountainous area of Paleogene, Panax is a floristic and fatty acids. The main aglycones of genus Panax are proto
composition and southwest China is known as the modern distribution panaxadiol, protopanaxatriol, oleanolic acid and ocotillol. Despite si
center (Wang, 2001). milar components to some extent, their contents are different.
Panax is a kind of medicinal and edible tonic with a medicinal Genus Panax plants have been recognized as precious tonic Chinese
history of over four thousand years. It mainly regulates bodily func medicines since ancient times. However, the price of its medicinal
tions, prolongs lifespan and exerts antineoplastic and neuroprotective materials varies greatly by species and planting pattern, which is one of
functions, which is one of the reasons for the gradually increasing de the most important factors for the extensive studies on the plants. The
mand for genus Panax plant. The main medicinal part of Panax plant is summary of its abundant traditional uses, chemical constituents and
root. However, other various parts, including the leaves, flowers, rhi pharmacological activities can provide better guidance on the rational
zomes and fibrils, can also be used as medicines. Ginseng Radix et utilization of the genus Panax. In this review, a comprehensive com
Rhizoma, Ginseng Folium and Panax Japonicus Rhizome have been pilation is primarily made concerning the botany information, phy
officially recorded in Chinese Pharmacopoeia (2015 edition) and tochemistry, traditional uses and bioactivities of genus Panax. The
Japanese Pharmacopoeia (17 edition) (Commission, 2015; Ri, 2016). compounds that were found in Panax plants in the past 60 years, in
Based on recent studies, the aerial parts of this genus had different cluding their corresponding chemical structures and biological activ
pharmacological activities and chemical components from those of ities were mainly introduced. We aim to provide potential development
rhizomes, which was similar to the expression of the ancient classical value to analyze metabolic mechanism of its important natural products
monograph (Bai et al., 2014). “Ben Cao Gang Mu Shi Yi” (On Supple and to discover new drugs. Moreover, a more comprehensive review of
ment to Compendium of Material Medica), a classical Chinese structure-activity relationships of chemical components will provide
2
certain theoretical basis for the quality control and rational use of genus reputation among consumers. In terms of processing and administra
Panax. tion, P. ginseng is usually sliced and dried. It can also be directly chewed
after peeling fresh roots or soaked in wine for drinking and chewing.
2. Materials and methods P. ginseng is usually boiled with chicken in China and Korea and made
into energy drinks, tea varieties, or candies in America as well (Wu and
The available information about genus Panax was collected via Web Kang, 2019). However, most of them are mainly used medicinally, and
of Science, Google Scholar, PubMed, Baidu Scholar, Science Direct, the traditional Chinese medicine preparations represented by oral li
China National Knowledge Infrastructure (CNKI), and Springer search. quid are especially popular among women in Japan.
The keywords used include Panax, saponin, secondary metabolites, P. quinquefolius possesses a medicinal history of over 300 years in
chemical components, biological activity, pharmacology, traditional China. The earliest record found in the literature was “Ben Cao Gang
medicinal uses, safety, and other related words. The Plant List (www. Mu” (General Outline of Materia Medica) by Li Shizhen, demonstrating
theplantlist.org) and Catalogue of Life: 2019 Annual Checklist (www. that P. quinquefolius was bitter in taste and cool-natured. It was mainly
catalogueoflife.org/col/) databases were used to verify the scientific used to remove pathogenic fire, generate body fluid and eliminate
names and provide subspecies classification and distribution informa tiredness, especially for patients with dryness-heat constitution. Zhang
tion of Panax. Xichun, a famous modern doctor, discussed P. quinquefolius in his book
“Yi Xue Zhong Zhong Can Xi Lu” (in Chinese). Specifically, Zhang et al.
3. Botanical studies reported that P. quinquefolius was a cool-natured herb with the function
of supplementing energy and promoting blood circulation (Zhang,
According to Flora of China, Panax belongs to perennial herbs with 2001). People who cannot use P. ginseng as tonics can use P. quinque
one stalk having palmately compound leaves, and erect stems without folius as a substitute. Another effect of P. quinquefolius is to treat he
branches. Panax is a self-pollinated plant that blooms at the third year matochezia, which was found in Japanese Medical Book “Lei Ju Yao
of growth with a solitary inflorescence arranged in terminal umbels. Fang” (in Chinese). In general, P. quinquefolius is administered at a dose
When flowers bloom in May, they grow into red globose berries. Ovoid of 3–5 g per day, which can be added or subtracted appropriately ac
seeds are collected from the red berries with two pale yellow seeds in cording to different disease conditions. P. ginseng in the original pre
each fruit. The roots are fleshy and spindle-shaped with two or five scription of TCMs of Qing Shu Yi Qi Tang was replaced by P. quinque
rootlets and root hairs. The rhizome (neck) is considered as the im folius, which was used clinically in combination with TCMs to treat
portant identifier that determines plant quality. (Flora of China children with summer heatstroke and other symptoms (Wang, 1852).
Editorial Committee, 2001; Lan, 1978). Originated from the remnants of the Tertiary ancient tropical
Genus Panax can be divided into two groups. The first group is mountains 25 million years ago, P. notoginseng was taken as the most
characterized by short rhizomes, fleshy roots and large seeds, with precious Chinese medicine in Ben Cao Gang Mu (Compendium of
tetracyclic triterpene dammarane-type saponins as its characteristic Materia Medica). The application of P. notoginseng was first recorded in
chemical components. As one of the ancient taxa, it is characterized by the “Xian Zhuan Wai Ke Mi Fang” (in Chinese), which had been nearly
narrow or intermittent distribution on geographical distribution. 600 years. At the beginning of the 20th century, Qu Huanzhang, a folk
Moreover, P. ginseng, P. quinquefolius and P. notoginseng are regarded as doctor, used P. notoginseng as one of the main ingredients to invent the
typical plants. The second group is morphologically characterized by famous Yunnan Baiyao. It was used for trauma and various hemor
long rhizomes, underdeveloped or incomplete fleshy roots and small rhagic diseases largely due to remarkable curative effect (Zhou et al.,
seeds, rich in pentacyclic triterpene oleanolic saponin, with extensive 2017). In TCMs, raw P. notoginseng is used for hemostasis and pro
and continuous geographical distribution. As an evolutionary group, its moting blood circulation while processed P. notoginseng is used for
representative plants contain P. japonicas, P. notoginseng. and improving immunity. That is so-called “fresh hits cooked tonic” (Zhao,
P. pseudoginseng, belonging to the first group in morphology. However, 2018). Meanwhile, edible P. notoginseng has a long history in China.
its chemical components are consistent with those in the second group, Among the wide variety of P. notoginseng-related food (including P. no
which is recognized as a transitional group between the two groups (Lu toginseng stewed chicken, P. notoginseng root fried meat and P. noto
et al., 1992). ginseng tea), it is worthwhile to mention that the P. notoginseng vinegar
can be used as not only seasonings but also direct health supplements
4. Traditional uses (Wu and Kang, 2019). The annual sales income of P. notoginseng pro
ducts is nearly $14.6 million, and it is exported to the Asian and Eur
TCMs advocates individualized therapy, mainly by using Chinese opean countries as food additives. Table 2 presents the traditional uses
herbal medicine to determine the specific type of syndromes and to (edible and medicinal use) of P. ginseng, P. quinquefolius and P. noto
modulate human balance. As a significant species of genus Panax, ginseng.
P. ginseng has been considered as an emblematic plant in folk medicine
since ancient times, with recorded nature since two thousand years ago. 5. Chemical components
According to “Shen Nong Ben Cao Jing” (Shen Nong's Herbal), P. ginseng
harbors diverse pharmacological effects, such as nourishing, in The chemical components of genus Panax (as shown in Table S1.)
telligence improving, mind tranquilizing, eyesight improving and anti- include saponins (1–516), phytosterols (517–523), flavonoids
aging activities. P. ginseng returns to the spleen meridian, which is the (524–545), polyacetylenes (546–568), polysaccharides (569–598),
key medicine for invigorating the spleen (Tao, 1994). It is often com fatty acids (599–621), glycosides (622–627), coumarins (628–630),
patible with TCMs Astragali Radix, Atractylodes Macrocephalae Rhi polyphenols (631–632), phenolic acids (633–643), sulfonic acids
zoma and other qi-invigorating and spleen-invigorating drugs for fever, (644–647), aldehydes (648), ketones (649–650), lactams (651–655),
high humidity, diabetes, etc. (Lan, 1978). In addition, P. ginseng is also amino acids (656–673), inorganic elements (674–735) and cyclic di
used to treat hemorrhage and impotence, and to treat critically ill pa peptides (736–748).
tients with double dose or compatibility with aconitum roots (Park Studies on the chemical components of Panax plants can be tracked
et al., 2012). However, P. ginseng cannot be used in combination with back to the mid-19th century. In 1985, the first ginsenoside “pana
Radix et Rhizoma Veratri Nigri or Faeces trogopterori (the dry excre quilon” was isolated from P. quinquefolius by Garrignes S (Taik-Koo Yun
ment of Trogopterus xanthipes) (Jia et al., 2009). P. ginseng and its pro et al., 2001). Since 1970s, some new species of genus Panax (e.g.
ducts, as the potent natural tonics, rank among the top ten in the nat P. vietnamensis Ha et Grushv. and P. sokpayensis) have gradually at
ural medicine market in Europe and America, which have earned a high tracted the attention of researchers (Duc et al., 1994; Sharma and
3
L. Liu, et al.
Table 2
The traditional uses of P. ginseng, P. quinquefolius and P. notoginseng.
Panax plants Edible methods Edible products Classical prescriptions in Traditional and clinical uses Origin
China
P. ginseng Chewing; brewing tea; stewing; Active ginseng instant tablets; ginseng nectar; ginseng Bu zhong yi qi tang (补中益 Curing for the weakness of spleen and "Pi wei lun" (Treatise on the spleen and
steaming; making porridge; wine; active ginseng sugar; ginseng coffee; ginseng pork; 气汤)∗ stomach, kidney-Yang deficiency. stomach)
grinding powder; brewing wine ginseng protein preserved beans; shenrong tonic wine Li zhong wan (理中丸)∗ Curing for digestive system disorders such "Shanghan lun" (Treatise on treatment of
as loss of appetite, nausea, burping, diseases induced by cold)
vomiting, or diarrhea
Si jun zi tang (四君子汤)∗ Curing for chronic gastric ulcer and peptic "Taiping Huimin Hejiju Fang" (Formulary of
ulcer disease the people's benevolent pharmacy of the
Taiping era)
Gui pi tang (归脾汤)∗ Curing for mental agitation, anxiety, and "Ji sheng fang" (Prescriptions for succouring
insomnia (guipi = restore the spleen) the sick)
P. quinquefolius American ginseng buccal tablet; American ginseng qingrun Qing shu yi qi tang (清暑益 Clearing heat and detoxicating, invigorating "Pi wei lun" (Treatise on the spleen and
气汤)∗
4
tea; American ginseng powder; American ginseng drink strength and spleen nutrition stomach)
Yang shen bao fei wan (洋参 Curing the swell of throat, dry mouth and Pharmacopoeia of PR China
保肺丸)∗ cough
Shen mai fu shen tang (参脉 Curing for the syndrome of dampness-heat "Wen re jing wei"
茯神汤)∗ due to spleen deficiency
Jia wei jie du sheng mai san Curing for the toxic shock syndrome caused "Qian jia miao fang"
(加味解毒生脉散)∗ by escherichia coli septicemia
P. notoginseng Shenqi buccal tablet; radix notoginseng seasoning; radix An shen zhi tong tang (安神 Curing for excruciating pain caused by "Lin ru gao gu shang yan fang ge jue fang
notoginseng flower tea; radix notoginseng powder; radix 止痛汤)∗ serious injury and restlessness jie"
notoginseng wine Hua xue dan (化血丹)∗ Curing for hemoptysis, hematuria and "Yi xue zhong zhong can xi lu"
hematochezia
Fu fang xue shuan tong jiao Curing for coronary heart disease stable Pharmacopoeia of PR China
nang (复方血栓通胶囊)∗ angina pectoris and early diabetic
nephropathy
Die da huo xue san (跌打活 Curing for falls, contusions, or sprains Pharmacopoeia of PR China
血散)∗
Note. ∗Cited from the website: https://www.wiki8.com/.

Pandit, 2009). At the same time, two-dimensional nuclear magnetic and P. japonicus. It was found that most of the saponins in the aerial
resonance (2D NMR) and quadrupole time of flight mass spectrometer parts of Panax plants were dammarane-type saponins and ocotillol-type
(Q-TOF-MS) were used as the promising technique for identifying saponins. Structurally speaking, triterpenoid saponins can be divided
chemical compounds of genus Panax and clarifying stereo configura into tetracyclic triterpene saponins (e.g. dammaran-type) and penta
tions (Ma et al., 1999; Wang et al., 2016a,b,c,d). From 1970 to 2000, cyclic triterpene saponins (e.g. oleanolic-type and ocotillol-type sapo
the reported saponins compounds mostly belonged to C17 side chain nins) according to the different aglycones. Protopanaxatriol (PPT) sa
varied type. However, due to the substitution of –OH and –OOH, the ponins and protopanaxadiol (PPD) saponins belong to dammarane-type
absolute configuration of some chiral carbon atoms has not been solved. saponins which have 1–4 glycosyl groups combined with their agly
Since 2000, various new saponins had been isolated with the devel cones in general. They were considered as one of the main active
opment of chromatography, spectroscopy and mass spectrometry, components of Panax. In PPD type saponins, the sugar chains are
making it possible to rapidly screen natural products of Panax. Yao usually connected with C3 or C4 position of aglycones while PPT
et al. constructed a two-dimensional liquid chromatography (2D-LC) aglycones are usually linked to the C6 or C20 position. In this way, a
separation system based on high-performance liquid chromatography- variety of saponins are formed due to the different types of glycosyl
high resolution mass spectrometry (HPLC-HRMS) platform to identify groups and the linking orders such as PPT saponins Re, Rf and Rg1 and
945 ginsenosides in the leaves of P. notoginseng and inferred 662 gin PPD saponins Rb1, Rb2, Rc and Rd. The number of hydroxyl groups
senosides to be the new ones (Yao et al., 2014). Chen et al. established a showed a decreasing trend of Rb1 > Rb2 = Rc > Rd =
method for nondestructive differentiation of Panax species (including Re > Rg1 = Rf by comparing the molecular structures of ginsenosides,
America ginseng and Asian ginseng) by visible and short-wave near- which may be the key to their differences in bioactivities. The saponins
infrared spectroscopy (Vis-SWNIR) (Chen et al., 2011). Spectral ana isolated from different parts of Panax plants are summarized as follows
lysis is becoming increasingly as a key technology for the quality con (Tables 3–9).
trol of genus Panax owing to the advantage of being rapid, non-de
structive and cost-effective. Fig. 1 exhibites the trend of annually 5.1.1. Protopanaxadiol type saponins (PPD, 1–94)
reported new saponins from the Panax genus within the time Among all the discovered dammarane tetracyclic triterpene sapo
1978–2019. nins of genus Panax, 94 saponins are classified as PPD type and 93
saponins are classified as PPT type according to whether there is hy
5.1. Saponins (1–516) droxyl on the C-6 site. In the PPDs, the sugar moieties are attached to
the C3 and/or C20 in the ring of the triterpene dammarane (as in Rg3,
Saponins are complex glycosides composed of steroids or triterpe Rb1, Rb2, Rc and Rd), while acylation of 6-OH of glucose tends to occur
noid glycosides ligands and sugar chains. They are mainly distributed in at the end of the 3-sugar chain. It can be confirmed that acylation has
terrestrial higher plants, such as P. ginseng, and exerted extensive become an important source of new structures in the PPDs. For ex
pharmacological activities. In ancient folk medicine, they were used as ample, six new acylated PPD type ginsenosides (Ra4–Ra9) (7–12) were
hemolytic agents, antimicrobial agents and anti-inflammatory agents isolated from the roots of P. ginseng, which were very minor acylated
(María et al., 2015). However, the saponins exhibited effective activ ginsenosides of genus Panax (Zhu et al., 2011). In these ginsenosides,
ities are hydrolyzed aglycones or secondary glycosides. the 4-OH in the terminal glucose of ginsenoside Ra8 was acylated.
Among the 18 species of genus Panax, P. ginseng, P. quinquefolius and Ginsenoside Rs2 (24) (Tung et al., 2010a,b) and Rs3 (25) (Baek et al.,
P. notoginseng with similar genetic relationships take dammarane-type 1997) were acetylated ginsenosides of ginsenoside Rc, and 20(S)/(R)
ginsenosides as main effective components. In addition, the content of Rg3, respectively. In addition, it reported that malonyl-substitution was
saponins is affected by species, parts, growing period and producing the unique polar acylation mode, such as m-Ra3 (27) (Ruan et al.,
area, which means their pharmacological activities are not identical. 2010), m-Rb1 (28), m-Rb2 (29), m-Rc (30), m-Rd (31) (KITAGAWA
Bai et al. (2014) reviewed the saponins in the aerial parts (stems, et al., 1989) and m-notoginoside R4 (32) (Sun et al., 2007), which are
leaves, flowers and fruits) of P. ginseng, P. notoginseng, P. quinquefolius easily hydrolyzed from dry green parts of ginseng into Rb1, Rb2, Rc and
Fig. 1. The cumulative histogram plotting the number of annually reported new saponins from 1978 to 2019.
5
Table 3
The structure of protopanaxadiol type saponins.
PPD type saponins core structure
NO. Compound R1 R2 R3 R4 C20
1 20(S)-25-OCH3-PPD H OH OH OCH3 S
2 20(R)-Protopanaxadiol H OH OH CH3 S
3 20(S)- Protopanaxadiol H OH CH3 OH R
4 Ginsenoside Ra1 Glc2-Glc OH O-Glc6-Ara(p)4-Xyl CH3 S
5 Ginsenoside Ra2 Glc2-Glc OH O-Glc6-Ara(f)2-Xyl CH3 S
6 Ginsenoside Ra3 Glc2-Glc OH O-Glc6-Glc3-Xyl CH3 S
7 Ginsenosides Ra4 S5 OH O-Glc6-Ara(p)4-Xyl CH3 S
8 Ginsenosides Ra5 S6 OH O-Glc6-Ara(p)4-Xyl CH3 S
9 Ginsenosides Ra6 S5 OH O-Glc6-Glc CH3 S
10 Ginsenosides Ra7 S5 OH OGlc6-Ara(f) CH3 S
13 Ginsenoside Rb1 Glc2-Glc OH O-Glc6-Glc CH3 S
14 Ginsenoside Rb2 Glc2-Glc OH O-Glc6-Ara(p) CH3 S
15 Ginsenoside Rb3 Glc2-Glc OH O-Glc6-Xyl CH3 S
16 Ginsenoside Rc Glc2-Glc OH O-Glc6-Ara(f) CH3 S
17 Ginsenoside Rd Glc2-Glc OH O-Glc CH3 S
18 20(S)-Ginsenoside Rg3 Glc2-Glc OH OH CH3 S
19 20(R)-Ginsenoside Rg3 Glc2-Glc OH CH3 OH R
20 20(S)-ginsenoside Rh2 Glc OH OH CH3 S
21 20(R)-ginsenoside Rh2 Glc OH CH3 OH R
22 Ginsenoside F2 Glc OH O-Glc CH3 S
23 Ginsenoside Mc H OH O-Glc6-Ara(f) CH3 S
24 Ginsenoside Rs2 Glc2-Glc6-AC OH O-Glc2-Ara(f) CH3 S
25 Ginsenoside Rs3 Glc2-Glc-(6-O-AC) OH OH CH3 S
26 6″-Acetyl-ginsenoside-Rd Glc2-Glc6-COCH3 OH O-Glc CH3 S
27 Malonyl ginsenoside Ra3 Glc2-Glc-COCOCH2O OH O-Glc6-Glc3-Xyl CH3 S
28 Malonyl ginsenoside Rb1 Glc2-Glc-(6-O-Mal) OH O-Glc6-Glc CH3 S
29 Malonyl ginsenoside Rb2 Glc2-Glc-(6-O-Mal) OH O-Glc6-Ara(p) CH3 S
30 Malonyl ginsenoside Rc Glc2-Glc-(6-O-Mal) OH O-Glc6-Ara(f) CH3 S
31 Malonyl ginsenoside Rd Glc2-Glc-(6-O-Mal) OH O-Glc CH3 S
32 Malonyl notoginsenoside R4 Glc2-(6-Mal)Glc OH O-Glc6-Glc6-Xyl CH3 S
33 Notoginsenoside Fa Glc2-Glc2-Xyl OH O-Glc6-Glc CH3 S
34 Notoginsenoside Fc Glc2-Glc2-Xyl OH O-Glc6-Xyl CH3 S
35 Notoginsenoside Fe Glc OH O-Glc6-Ara(p) CH3 S
36 Notoginsenoside Ft1 Glc2-Glc2-Xyl OH OH CH3 S
37 Notoginsenoside FP2 Glc2-Glc2-Xyl OH O-Glc6-Ara(p) CH3 S
38 Notoginsenoside D Glc2-Glc2-Xyl OH O-Glc6-Glc6-Xyl CH3 S
39 Notoginsenoside K Glc6-Glc OH O-Glc CH3 S
40 Notoginsenoside L Glc2-Xyl OH O-Glc6-Glc CH3 S
41 Notoginsenoside O Glc OH O-Glc6-Xyl3-Xyl CH3 S
42 Notoginsenoside P Glc OH O-Glc6-Xyl4-Xyl CH3 S
43 Notoginsenoside Q Glc2-Glc2-Xyl OH O-Glc6-Xyl4-Xyl CH3 S
44 Notoginsenoside S Glc2-Glc2-Xyl OH O-Glc6-Ara(f)5-Xyl CH3 S
45 Notoginsenoside T Glc2-Glc2-Xyl OH O-Glc6-Glc3-Xyl CH3 S
46 Notoginsenoside R4 Glc2-Glc OH O-Glc6-Glc6-Xyl CH3 S
47 Notoginsenoside ST4 Glc2-Glc2-Xyl OH OH CH3 S
48 Notoginsenoside FZ Glc2-Glc2-Xyl OH O-Glc6-Ara(p) CH3 S
49 Notoginsenoside Fh1 Glc2-Glc2-Xyl OH O-Glc6-Ara(p)4-Xyl CH3 S
50 Notoginsenoside L5 S4 OH O-Glc6-Ara(f) CH3 S
51 Notoginsenoside L6 S4 OH O-Glc6-Ara(p) CH3 S
52 Notoginsenoside L7 S4 OH O-Glc6-Xyl CH3 S
53 Notoginsenoside L8 S4 OH O-Glc6-Glc CH3 S
54 Gypenoside IX Glc OH O-Glc6-Xyl CH3 S
55 Gypenoside V Glc2-Glc OH O-Glc6-Rha CH3 S
56 Gypenoside XVII Glc OH O-Glc6-Glc CH3 S
57 Gypenoside XIII H OH O-Glc6-Xyl CH3 S
58 Chikusetsusaponin VI Glc-Xyl6-Xyl OH O-Glc-Glc6 CH3 S
59 Chikusetsusaponin III Glc-Glc6-Xyl OH OH CH3 S
60 Chikusetsusaponin VII Glc6-Xyl OH O-Glc6-Glc CH3 S
(continued on next page)
6
Table 3 (continued)
NO. Compound R1 R2 R3 R4 C20
6 2 6
61 Chikusetsusaponin FK4 Xyl- Glc -Glc OH O-Glc -Ara(f) CH3 S
62 Chikusetsusaponin FK5 Xyl-6Glc2-Glc OH O-Glc6-Xyl CH3 S
63 Chikusetsusaponin FK6 Xyl-6Glc2-Glc OH O-Glc CH3 S
64 Chikusetsusaponin FK7 Glc2-Glc O-Glc OH CH3 S
65 Quinquenoside I S1 OH O-Glc CH3 S
66 Quinquenoside II S2 OH O-Glc6-Glc CH3 S
67 Quinquenoside III S3 OH O-Glc CH3 S
68 Quinquenoside V Glc2-Glc OH O-Glc6-Glc4-Glc CH3 S
69 Quinquenoside L2 Glc2-Glc OH O-Glc CH3 S
70 Quinquenosides L10 Glc OH O-Glc6-Ara(p) CH3 S
71 Quinquenosides L14 Glc2-Glc OH O-Ara(p) CH3 S
72 Quinquenosides L16 Glc2-Glc OH O-Glc6-Glc CH3 S
73 Compound O Glc OH O-Glc2-Ara(p) CH3 S
74 Compound K H OH O-Glc CH3 S
75 Compound Y H OH OH CH3 S
76 Pseu-ginsenoside Rc1 Glc2-Glc6-AC OH O-Glc CH3 S
77 Yesanchinoside J Glc2-Glc6-AC OH O-Glc6-Glc6-Xyl CH3 S
78 Vinaginsenoside R16 Glc2-Xyl O-Glc OH CH3 S
79 Vinaginsenoside R3 Glc2-Glc H O-Glc CH3 S
80 Quinquenoside Jb Glc2-Glc OH O-Glc6-Glc6-Ara(f) CH3 S
81 20(R)methoxyl-ginsenoside Rg3 Glc2-Glc OH OCH3 CH3 R
82 20(S)methoxyl-ginsenoside Rg3 Glc2-Glc OH OCH3 CH3 S
83 Malonyl-floralginsenosides Rb1 Glc2-Glc H O-Glc6-(4-Mal)Glc CH3 S
84 Malonyl-floralginsenosides Rb2 Glc2-(3-Mal)Glc H O-Glc6-Glc CH3 S
85 Malonyl-floralginsenosides Rd1 Glc2-(2-Mal)Glc H O-Glc CH3 S
88 Malonyl-floralginsenosides Rd4 Glc2-Glc H O-(3-Mal)Glc CH3 S
89 Malonyl-floralginsenosides Rd5 Glc2-Glc H O-(6-Mal)Glc CH3 S
90 Malonyl-floralginsenosides Rd6 Glc2-(6-Mal)Glc H O-(6-Mal)Glc CH3 S
91 Malonyl-floralginsenosides Rc1 Glc2-(6-Mal)Glc H O-Glc6-Xyl CH3 S
92 Malonyl-floralginsenosides Rc2 Glc2-(4-Mal)Glc H O-Glc6-Ara(p) CH3 S
93 Malonyl-floralginsenosides Rc3 Glc2-(3-Mal)Glc H O-Glc6-Ara(p) CH3 S
94 Malonyl-floralginsenosides Rc4 Glc2-(3-Mal)Glc H O-Glc6-Ara(f) CH3 S
Note: Glc: β-D-glucopyranosyl; Glc∗: α-D-glucopyranosyl; Xyl: β-D-xylopyranosyl; Ara(p): α-D-arabinopyranosyl; Ara(f): α-L-arabinofuranosyl; Rha: α-L-rhamno
pyranosyl; AC: acetyl; Mal: malonyl.
Rd (Wang, 2001). Pseu-ginsenoside Rc1 (76) and yesanchinoside J (77) glycosyl chains and the presence of an inner glucuronic acid (GlcA)
were isolated from P. ginseng and P. japonicus respectively, with the residue attached to C-3. Ginsenoside Ro, belonging to oleanane-type
same acylation mode as Rg3. The structures of parent nucleus and re pentacyclic triterpene, is considered to be synthesized from oleanolic
lated compounds in PPD type saponins are shown in Table 3. acid. It was found only at low levels in P. ginseng. Yang et al. isolated
two oleanolic acid type saponins (stipuleanoside R1 209, R2 210) from
5.1.2. Protopanaxatriol type saponins (PPT, 95–187) the rhizome of P. stipuleanatus for the first time (Shukla et al., 1992).
As a class of saponins with important biological activities, 93 kinds Stipuleanoside R2 could be converted to R1 by potassium hydroxide-
of PPT type saponins have been reported so far. In the PPT type sapo methanol saponification, or turned into chikusetsusaponin IV by at
nins, the sugar moieties are attached to the ring at the C6 (as in Rg1, Re taching a portion of the β-D-glucopyranosyl group at the C3 position of
and Rg5) and C20 position normally. Ginsenoside Re1 (105) and Re2 its glucuronic acid. Bifinosides A-C (198–200) were isolated from the
(106) are the first example of ginsenosides moiety containing [α-D- polar fractions of a methanol extract of P. bipinnatifidus roots (Nguyen
glucopyranosyl-(1 → 3)-β-D-glucopyranosyl] isolated from the genus et al., 2011). Furthermore, a liquid chromatography-tandem mass
Panax (Wang et al., 2013a,b). In addition, some interesting studies spectrometry (LC-MS/MS) method was established to determine the
showed that the substitution of malonyl or acetyl at C-60 or C-3 position natural compounds pseudoginsenoside RT1 butyl ester, taibaienoside I
could increase the antiproliferative activity by comparing the ginse (201), and chikusetsusaponin-IVa butyl ester (206), which were dif
noside Rh24 (111) and ginsenoside Rh26 (115) (Li et al., 2018). 20(S)- ferent from the artifactual compounds containing a butylester group
sanchirhinosides A1-A6 (160–165) as minor PPT type saponins were (Chan et al., 2011). The structures of parent nucleus and related com
isolated from the root extract of P. notoginseng. The olefine acid ester pounds in oleanolic acid type saponins are shown in Table 5.
group and acetyl were attached to the sugar chain of C-6 position of
160 and 161 respectively, which might be related to inhibit mi 5.1.4. Ocotillol type saponins (OT, 221–243)
tochondrial oxidative stress (Zhang et al., 2013). Qiu et al. (2017) ob Ocotillol type saponin is a class of tetracyclic triterpene saponins
tained 15 new malonyl-substituted triterpenoid saponins from the containing furan ring in the side chain, which are only found in a few
flower buds of P. ginseng including malonyl-floralginsenosides Re1–Re3 natural products, such as P. pseudoginseng, P. quinquefolius,
(178–180), through the Liquid chromatography -Mass spectrometry P. vietnamensis and P. japonicus. Botanical natural ocotillol-type sapo
(LC-MS)-guided phytochemical isolation. The structures of parent nu nins mainly include pseudoginsenoside F11 (PF11, 225), pseudo-ginse
cleus and related compounds in PPT type saponins are shown in noside RT5 (229), RT2 (230), RT4 (236), vina-ginsenoside R1 (VR1,
Table 4. 231), VR2 (232), VR5 (233), VR6 (234), VR13 (235), majonoside R1
(MR1, 239) and yesanchinoside A-C (241–243). The PF11 and RT5 in
5.1.3. Oleanolic acid type saponins (OA, 188–210) the ocotillol-type ginsenosides are the main characteristic compounds
The OA saponins are minor ginsenosides with a total of thirty-four of P. quinquefolius different from the P. ginseng. VR1 (231) and VR2
known compounds. They are characterized by C-3- and/or C-28- (232) were ocotillol saponins with an acetyl group on the sugar chain at
7
Table 4
The structure of protopanaxatriol type saponins.
L. Liu, et al.
PPT type saponins core structure
NO. Compound R1 R2 R3 R4 R5
95 20(S)- protopanaxatriol H H H OH CH3

96 20(R)-protopanaxatriol H H H CH3 OH
97 Ginsenoside Rg1 H Glc H O-Glc CH3
98 20(S)-ginsenoside Rg2 H Glc6-Rha H OH CH3
99 20(R)-ginsenoside Rg2 H Glc6-Rha H CH3 OH
100 20(S)-ginsenoside Rh1 H Glc H OH CH3
101 20(R)-ginsenoside Rh1 H Glc H CH3 OH
102 Ginsenoside Rf H Glc2-Glc H OH CH3
103 Ginsenoside F1 H H H O-Glc CH3
104 Ginsenoside Re H Glc2-Rha H O-Glc CH3
105 Ginsenoside Re1 H Glc H O-Glc3-Glc CH3
106 Ginsenoside Re2 H Glc3-Glc H O-Glc CH3
107 Ginsenoside Re3 H Glc H O-Glc4-Glc CH3
108 Ginsenoside Re4 H Glc H O-Glc6-Ara(f) CH3
8
109 Ginsenoside F3 H H H O-Glc6-Ara(p) CH3
110 Ginsenoside F5 H H H O-Glc6-Ara(f) CH3
111 Ginsenoside Rh24 H Ara(p)6-Rha H O-Glc CH3
112 Ginsenoside Rg18 H Glc H O-Glc2-Rha CH3
113 Ginsenoside Rs11 H Glc2-OGlc6-AC H O-Glc6-Ara(f) CH3
114 Ginsenoside Rh25 O-Xyl-Glc2 H H O-Ara-Glc6 CH3
115 Ginsenoside Rh26 O-(E)-but-2-enoyl-Glc-Glc2 H H O-Glc CH3
116 Ginsenoside Re5 H Glc2-Glc H OH CH3
117 Ginsenoside Mb Glc H H O-Glc6-Ara(p) CH3
118 20(R)-ginsenoside Rh19 Glc H H CH3 OH

119 Notoginsenoside R1 H Glc2-Xyl H O-Glc CH3
120 20(R)-Notoginsenoside R2 H Glc2-Xyl H CH3 OH
121 Notoginsenoside R3 H Glc H O-Glc6-Glc CH3
122 Notoginsenoside R6 H Glc H O-Glc6-Glc∗ CH3
123 Notoginsenoside N H Glc4-Glc∗ H O-Glc CH3
124 Notoginsenoside Rt H Glc6-OAC H O-Glc CH3
125 Notoginsenoside FP1 H Glc H O-Glc6-Ara(p) CH3
126 Notoginsenoside Rw1 H Xyl H O-Glc6-Xyl CH3
127 Notoginsenoside Fh7 H Glc2-Glc H O-Glc6-Glc CH3
128 Notoginsenoside M H Glc6-Glc∗ H O-Glc CH3
129 Notoginsenoside L4 S1′ H H O-Glc OH
130 Notoginsenoside L9 S4 H H O-Glc6-Ara(f) CH3
131 Notoginsenoside L10 S4 H H O-Glc6-Ara(p) CH3
132 Notoginsenoside L11 S4 H H O-Glc6-Xyl CH3
133 Notoginsenoside L12 S4 H H O-Glc6-Glc CH3
134 Chikusetsusaponin LM1 H H H O-Glc6-Xyl CH3
135 Chikusetsusaponin LM2 H H H O-Glc6-Xyl3-Xyl CH3
136 Chikusetsusaponin LM3 H H H O-Glc6-Ara(p)4-Xyl CH3
Table 4 (continued)
NO. Compound R1 R2 R3 R4 R5
L. Liu, et al.
2
137 Chikusetsusaponin LM4 Glc -Glc H Glc OH CH3
138 Chikusetsusaponin LM5 Glc2-Glc H H O-Glc6-Ara(f) CH3
139 Chikusetsusaponin LM6 Glc2-Glc H H O-Glc6-Ara(p)4-Ara(f) CH3
140 Chikusetsusaponin FK1 Glc2-Rha Glc H CH3 CH3
141 Chikusetsusaponin L10 H H Glc OH CH3
142 Chikusetsusaponin L5 H H H O-Glc6-Ara(p)4-Xyl CH3
143 3-acetyl ginsenoside F1 AC H H O-Glc CH3
144 6′-acetyl-ginsenoside F1 H H H O-Glc6-AC CH3
145 3β-acetoxyl ginsenoside F1 COO H H O-Glc CH3
146 6′-acetyl ginsenoside Rg3 H Glc2-Glc2 H O-Glc6-AC CH3
147 20-O-Gluco-ginsenoside Rf H Glc2-Glc H O-Glc CH3
148 6′-malonyl formyl-ginsenoside F1 H H H O-Glc CH3
149 6′-emalonyl formyl ginsenoside F1 H H H S2′ CH3
150 Pseudoginsenoside RT3 H Xyl H O-Glc CH3
151 Pseudo-ginsenosides F8 AC-6Glc2-Glc H H O-Glc6-Xyl CH3
152 Pseudoginsenoside Rs1 AC-6Glc2-Rha H H O–CH3 CH3
153 Floralquinquenosides E H Glc2-Rha H O-Glc6-Xyl CH3
154 Floralginsenoside M H Glc2-Rha H O-Glc6-Ara(f) CH3
155 Floralginsenoside N H Glc2-Rha H O-Glc6-Ara(p) CH3
156 Floralginsenoside P Glc2-Glc H H O-Glc6-Ara(p) CH3
157 Quinquenoside L17 H Glc H O-Glc6-Xyl CH3
158 Quinquenoside R1 Glc2-Glc6-AC H H O-Glc6-Glc CH3
159 Koryoginsenoside R1 H Glc6-Bu H O-Glc CH3
160 20(S)-sanchirhinosides A1 H S3′ H OH CH3
161 20(S)-sanchirhinosides A2 H S4′ H OH CH3
162 20(S)-sanchirhinosides A3 H Glc H O-Ara(p) CH3
9
163 20(S)-sanchirhinosides A4 H Ara(p) H O-Glc CH3
164 20(S)-sanchirhinosides A5 H Glc2-Ara(f) H O-Glc CH3
165 20(S)-sanchirhinosides A6 H Glc2-Xyl H O-Glc6-Glc CH3
166 6α-acetoxy-3β,12β,20R-trihydroxydammar-24-ene H OAC H CH3 OH
167 3-O-β-D-glucopyranosyl-20(S)-protopanaxatriol Glc H H OH CH3
168 3-formyloxy-20-O-β-D-glucopyranosyl-20(S)-protopanaxatriol S5′ H H O-Glc CH3
169 Vina-ginsenosides R4 Glc2-Glc H H O-Glc CH3
179 Vina-ginsenosides R7 Glc2-Glc-Xyl H H O-Glc CH3
171 Yesanchinoside D H Glc6-AC H O-Glc CH3
172 Yesanchinoside E Glc2-Rha H H CH3 O-Glc6-Xyl
173 20(R)-ginsenoside Rh5 OH O-Glc H CH3 O–CH3
174 6-O-[β-D-glucopyranosyl-(1 → 2)-β-D-glucopyranosyl]-20-O-[β-D-glucopyranosyl-(1 → 4)-β-D-glucopyranosyl]-20(S)-protopanaxatriol H Glc2-Glc H O-Glc4-Glc CH3
175 20(S)-6-O-[β-D-xylopyranosyl-(1 → 2)-β-D-xylopyranosyl]dammar-24-ene-3β,6α,12β,20-tetrol Xyl-Xyl2 H H OH CH3
176 Malonyl-ginsenoside Rg1 H Glc6-Mal H O-Glc CH3
177 Malonyl-ginsenoside Re H Glc2-Rha-Mal H O-Glc CH3
178 Malonyl-floralginsenosides Re1 H (6-Mal)Glc2-Rha H O-Glc CH3

179 Malonyl-floralginsenosides Re2 H Glc2-Rha H O-(2-Mal)Glc CH3
180 Malonyl-floralginsenosides Re3 H Glc2-Rha H O-(4-Mal)Glc CH3
181 20(R)-ginsenoside Rh1 6′-acetate H Glc6-Ac H CH3 OH
182 20(S)-ginsenoside Rh1 6′-acetate H Glc6-Ac H OH CH3
183 (20S)-20-O-[β-D-xylopyranosyl-(1 → 6)-β-D-glucopyranosyl-(1 → 6)-β-D-glucopyranosyl]dammar-24-ene-3β,6α,12β,20-tetrol H H H O-Xyl-Glc6-Glc6 CH3
184 (20S)-6-O-[(E)-but-2-enoyl-(1 → 6)-β-D-glucopyranosyl] dammar-24-ene-3β,6α,12β,20-tetrol H S3′ H OH CH3
185 Ginsenoside la Glc H H O-Glc CH3
186 Pseudo-ginsenoside RT8 Glc2-Glc H H CH3 CH3
187 Quinquenoside Ja H Glc2-Glc H O-Glc4-Glc CH3
Note: Glc: β-D-glucopyranosyl; Glc∗: α-D-glucopyranosyl; Xyl: β-D-xylopyranosyl; Ara(p): α-D-arabinopyranosyl; Ara(f): α-L-arabinofuranosyl; Rha: α-L-rhamnopyranosyl; AC: acetyl; Mal: malonyl.
Table 5
The structure of Oleanolic acid type saponins.
OA type saponins core structure
NO. Compound R1 R2 R3
188 Taibaienoside IV Glc-UA2-Glc CH3 H

189 Calenduloside E Glc-UA CH3 H
190 Oleanolic acid 3-O-[β-D-glucopyranosyl-(1 → 2)-β-D-glucuronopyranosyl-6′-O-n-butyl ester] I2 CH3 H
191 Calenduloside B Glc4-Gal CH3 Glc
192 Pjs-1 (oleanolic acid 28-O-β-D-glucopyranoside) H CH3 Glc
193 Pseudo-ginsenoside-RI3 I3 Xyl H
194 Pseudoginsenoside RP1 GlcUA2-Xyl CH3 H
195 Polyacetyleneginsenoside Ro I1 CH3 Glc
196 28-desglucosyl chikusetsusaponin IV GlcUA4-Ara(p) CH3 H
197 Oleanolic acid H CH3 H
NO. Compound R1 = I4 R2 R3
r1 r2 r3 r4
198 Bifinoside A Ara(p) H H COOCH3 CH3 H

199 Bifinoside B H Xyl6-Glc H COOCH3 CH3 H
200 Bifinoside C Xyl Ara(p) H COOCH3 CH3 Glc
201 Taibaienoside I H H Ara(f) n-Bu CH3 Glc
202 Chikusetsusaponin IV H H Ara(f) COOH CH3 Glc
203 Chikusetsusaponin IV methyl ester H H Ara(f) COOCH3 CH3 Glc
204 Chikusetsusaponin IVα H H H COOH CH3 Glc
205 Chikusetsusaponin IVa methyl ester H H H COOCH3 CH3 Glc
206 Chikusetsusaponin IVa butyl ester H H H n-Bu CH3 Glc
207 Chikusetsusaponin V H H Glc COOH CH3 Glc
208 Chikusetsusaponin Ib Ara(f) H H COOH CH3 Glc
209 Stipuleanoside R1 H Glc Ara(f) COOH CH3 H
210 Stipuleanoside R2 H Glc Ara(f) COOH CH3 Glc
211 Stipuleanoside R2 methyl ester H Glc Ara(f) COOCH3 CH3 Glc
212 Pseudoginsenoside RT1 Xyl H H COOH CH3 Glc
213 Pseudoginsenoside RT1 methyl ester Xyl H H COOCH3 CH3 Glc
214 Pseudoginsenoside Rp1 methyl ester Xyl H H COOCH3 CH3 H
215 Ginsenoside Ro Glc H H COOH CH3 H
216 Ginsenoside Ro methyl ester Glc H H COOCH3 CH3 Glc
217 Spinasaponin A 28-O-glucoside H Glc H COOH CH3 H
218 Araloside A methyl ester H H Ara(f) COOCH3 CH3 Glc
219 3-O-β-D-glucopyranosyl (1 → 3)-β-D-glucuronopyranoside-28-O-β-D-glucopyranosyl oleanolic acid methyl ester H Glc H COOCH3 CH3 Glc
220 3-O-β-D-xylopyranosyl (1 → 2)-β-D-glucopyranosyl-28-O-β-D-glucopyranosyl oleanolic acid Xyl H H CH2OH CH3 Glc
Notes: Glc: β-D-glucopyranosyl; Xyl: β-D-xylopyranosyl; Ara(p): α-D-arabinopyranosyl; Rha: α-L-rhamnopyranosyl; GlcUA: β-D-glucuronopyranosyl; Gal: D-glacto
pyranoside; Ara(f): α-L-arabinofuranosyl; n-Bu: n-butyl.
C-6, and were formulated as monoacetylated 24(S)-PF11 and mono chain varied saponins, compounds (350–360) were identified to pos
acetylated MR2 (Yamasaki, 2011). VR5 (233) and VR6 (234) were iso sess a C-24-OOH group. Studies showed that Rk1-Rk3 (426–428) were
lated from the rhizomes and roots of P. vietnamensis with an α-glucosyl isolated, which underwent a dehydration reaction of the 20-OH to form
moiety at the first time (Duc et al., 1994). The structures of parent a C-20 (21) double bond (Lee et al., 2017a,b). For these C17 side chain
nucleus and related compounds in ocotillol type saponins are shown in varied saponins, it remained to be solved that the absolute configura
Table 6. tion of chiral carbons with a hydroxylation or hydrogen peroxy sub
stitution at C-24 or C-23. Taking PPD or PPT saponin with a side chain
of 24-hydroxy-25-ene as an example, the absolute configuration of C-24
5.1.5. C-17 side chain varied saponins (244–464)
could be determined by comparing 13C NMR data of C-24 and C-26
This type of saponins is mainly C-17 side chain changes, including
(Yang et al., 2014).
C-24 (25) double bond displacement, hydroxylation, peroxidation, de
hydrogenation, cyclization and so on. The main structures of its parent
nucleus and C-17 side chain isomeric saponins reported so far are 5.1.6. Other structural saponins (465–516)
shown in Tables 7–8 In PPD type C-17 side chain varied saponins, In addition to the five types of saponins mentioned above, a total of
floranotoginsenoside A (246) was isolated from the flowers of P. noto 25 kinds of saponins containing isomeric sapogenins in genus Panax
ginseng, P. ginseng and P. quinquefolius with a C-23 (24) double bond and were summarized, and their specific structures are shown in Table 9.
the unconfirmed absolute configuration of C-25 (Seikou Nakamura, These new structural changes in saponins occur mainly in carbonylation
2007; Yoshikawa et al., 2007; Wang et al., 2009). In PPT type C-17 side of C-3 or C-18, dehydration between C-1 and C-2, C-5 and C-6, C-12 and
10
Table 6
The structure of Ocotillol type saponins.
OC type saponins core structure
NO. Compound R1 R2 R3 C20 C24
221 Gypenoside F11 H O-Glc-Rha CH3 R S

222 (20R,24R)-dammarane-20,24-epoxy-3β,6α,12β,25-tetraol H H CH3 R R
223 Vina-ginsenosides R14 H O-Glc2-Xyl CH3 S R
224 24(R)-Ocotillol H OH CH3 S R
225 Pseudoginsenoside F11 H O-Glc2-Rha CH3 S R
226 24(R)-majoroside R1 H OH CH3 S R
227 (20S,24R,25R)-6-O-[β-D-glucopyranosyl-(1 → 2)-β-D-glucopyranosyl]-dammar-20,24-epoxy-3β,6α,12β,25,26-pentaol H O-Glc2-Glc CH2OH S R
228 (20S,24R)-dammarane-20,24-epoxy-3β,6α,12β,25-tetraol H OH CH3 S R
229 Pseudoginsenoside RT5 H O-Glc CH3 S R
230 Pseudoginsenoside RT2 H O-Glc2-Xyl CH3 S R
231 (20S,24R)-Pseudoginsenoside F11 H O-Glc2-Rha CH3 S R
232 Vina-ginsenosides R1 H AC-Glc2-Rha CH3 S S
233 Vina-ginsenosides R2 H AC-Glc2-Xyl CH3 S S
234 Vina-ginsenosides R5 H Glc2-Xyl4-Glc CH3 S S
235 Vina-ginsenosides R6 H Glc6-Glc2-Xyl CH3 S S
236 Vina-ginsenosides R13 H Glc2-Xyl CH3 S S
237 (20S,24S,25R∗)-6-O-[β-D-glucopyranosyl-(1 → 2)-β-D-glucopyranosyl]-dammar-20,24-epoxy-3β,6α,12β,25,26-pentaol H Glc2-Glc CH2OH S S
238 Pseudo-ginsenoside RT4 H Glc CH3 S S
239 24(S)-majoroside R1 H Glc2-Glc CH3 S S
240 24(S)-6-O-[β-D-glucopyranosyl-(1 → 2)-β-D-glucopyranosyl]-dammar-20,25-epoxy-3β,6α,12β,24α-tetraol H Glc2-Glc CH3 S S

241 24(S)-Majoroside R2 H Glc2-Xyl CH3 S S
242 (20S,24S)-dammarane-20,24-epoxy-3β,6α,12β,25-tetraol H H CH3 S S
243 Yesanchinoside A (24S) H AC-6Glc2-Glc CH3 S S
244 Yesanchinoside B (24S) H Glc-6Glc2-Glc CH3 S S
245 Yesanchinoside C (24S) H Glc2-Glc2-Xyl CH3 S S
Note: Glc: β-D-glucopyranosyl; Xyl: β-D-xylopyranosyl; Rha: α-L-rhamnopyranosyl; AC: acetyl.
C-13, or further hydroxylation of C-7, C-15, C-16 and C-19-dehydrox 5.2. Phytosterols (517–523)
ylation. PPT saponins tend to lose H2O at C-6, forming a double bond
between C-5 and C-6. As a case in point, 5,6-didehydroginsenoside Rg3 Phytosterol is a kind of active ingredients, which widely exists in
(489), 5,6-didehydroginsenoside Rd (490) and 5,6-didehydroginseno roots, stems, leaves, fruits and seeds of plants. It is called “the key to
side Rb1 (491) derived from two species with a 5 (6) double bond and life” by scientists and has been recognized and applied in the field of
then further hydroxylated to notoginsenoside G (476), yesanchinoside food by forty-seven countries. Phytosterols have good antioxidant
G (477) and quinquenoside IV (478) (Yoshikawa et al., 1997, 1998; Zou properties and can be used as antioxidants and nutritional additives to
et al., 2002; Wan et al., 2010; Li et al., 2018). The only difference be inhibit the absorption of cholesterol and promote the degradation and
tween three new polyacetylenic oleanane-type triterpenoids (baisanqi metabolism of cholesterol. At present, no more than ten plant sterols
saponin A-C (465–467) and chikusetsusaponin Ivα (204) is the rare have been found in Panax. Wei et al. obtained β-sitosterol (518) from
panaxytriol moiety existed (Liu et al., 2016). Four new 19-dehydroxy- petroleum ether of the ethanol extract of P. notoginseng villus root and
PPD type saponins, including notoginsenoside I (479), yesanchinoside I β-sitosterol-D-glucoside from ether extract of P. notoginseng villus root
(480) and vina-ginsenoside R3 (481) were isolated from the roots of (Wei et al., 1980). A new sterol glucoside 3-O-β-D-glucopyranosyl-
P. notoginseng, P. japonicus, P. ginseng and P. quinquefolius respectively 5,22,24-stigmastatrienol (519), and a known sterol 5,22-stigmasta
(Yoshikawa et al., 1997; Wang et al., 1998; Zou et al., 2002; Ali and dienol (520) were isolated from seeds of P. ginseng and evaluated for
Sultana, 2016). Ginsenosides Rh18 (502) was isolated from the stems their inhibitory activities on tumor necrosis factor (TNF) by Kim et al.
and leaves of P. ginseng (Li et al., 2012), which could be considered as a (2013).
compound derived from a precursor with a 22 (23) double bond. It was
protonated to an allylic cation and then trapped by the 12-hydroxyl 5.3. Flavonoids (524–545)
group. The new lupane-triterpene compounds 3β-cis-feruloyloxy-16β-
hydroxylup-20 (29)-ene (474) and 3β-trans-feruloyloxy-16β-hydro The flavonoid is a kind of low molecular natural plant ingredient,
xylup-20 (29)-ene (475) were isolated from the ethyl acetate extract of and this kind of compound has a common parent nucleus C6–C3–C6. A
P. ginseng seeds. They showed effective inhibitory activity on neutrophil total of 22 flavonoids were collected in this study due to the limited
kernel factor kappa B (NF-κB) in HepG2 cells by decreasing the cellular reports on flavonoids of Panax. The study of flavonoids in P. notoginseng
concentrations of NO synthase (iNOS) and Cyclooxygenase-2 (COX-2) has started earlier. Flavonoids A and B were isolated from the villus
induced by inflammatory factors (Kim et al., 2012). roots of P. notoginseng for the first time by Wei et al., and identified as
quercetin (525) and quercetin glycoside respectively (Kim et al., 1989).
11
Table 7
The structure of PPD C17-side chain varied saponins.
L. Liu, et al.
PPD C17-side chain varied
12
NO. Type Compound R1 R2 R3 R4 Chiral Carbon
246 V1 25-hydroxy-23-ene-20(S)-protopanaxadiol H OH OH – C24:S

247 V1 Ginsenoside-M6a Glc2-Glc OH O-Glc – C25:S
248 V1 Floranotoginsenoside A Glc2-Glc OH O-Glc6-Ara(f) – C25:S
249 V1 Gypenoside XLIX Glc2-Glc OH O-Glc6-Xyl – C25:S
250 V1 Notoginsenoside L16 Glc OH O-Glc6-Ara(f) – C25:S
251 V1 Vina-ginsenosides R8 Glc2-Glc OH O-Glc – C25:R
252 V1 Dammar-23 (24)-ene-3β,12β, 20(S), 25-tetraol-20-O-β-D-glucopyranosyl-3-O-β-D-glucopyranoside Glc OH Glc – C25:R
253 V1 Majoroside F4 Glc OH O-Glc – C25:R
254 V1 dammar-23 (24)-ene-3β, 12β, 20(S), 25-tetraol–20-O-β-D-glucopyranoside H OH O-Glc – C25:R
255 V2 Notoginsenoside Fh6 Glc2-Gen OH O-Glc – –
256 V3 Notoginsenoside SFt2 Glc OH OH – –
257 V3 dammar-3β,12β,20(S),24(ζ),25-pentaol-20-O-β-D-glucopyranoside H OH O-Glc – –
258 V3 Chikusetsusaponin FM1 Glc2-Glc OH O-Glc2-Xyl – –
259 V4 Notoginsenoside R7 Glc OH – – –
260 V4 3β-acetoxy-12β-hydroxy-20 (R), 25-epoxy dammarane AC OH – – –
261 V5 Notoginsenoside SFt1 Glc OH OH – C24:R
262 V5 Notoginsenoside Fh3 Glc2-Glc2-Xyl OH O-Glc2-Xyl – C24:R
263 V5 Notoginsenoside Fh4 Glc2-Glc2-Xyl OH O-Glc6-Glc – C24:R
264 V5 Floranotoginsenoside D Glc2-Glc OH O-Glc6-Ara(f) – C24:R
265 V5 Notoginsenosides LK6 Glc2-Glc OH O-Xyl – C24:R
266 V5 Notoginsenosides LK7 Glc2-Glc OH O-Glc6-Ara(f) – C24:R
267 V5 Notoginsenosides LK8 Glc2-Glc2-Xyl OH OH – C24:R
Table 7 (continued)
NO. Type Compound R1 R2 R3 R4 Chiral Carbon

L. Liu, et al.
2
268 V5 Vinaginsenosides R9 Glc -Glc OH O-Glc – C24:S
269 V5 Bipinnatifidusoside F1 Glc2-Glc OH O-Glc – C24:R
270 V5 Majoroside F1 Glc2-Glc OH O-Glc – C24:R
271 V6 Notoginsenoside Ft2 Glc2-Glc2-Xyl OH OH – –
272 V7 Ginsenoside II Glc2-Glc OH O-Glc OH –
273 V7 Floranotoginsenoside B Glc2-Glc OH O-Glc2-Xyl OH –
274 V7 Floranotoginsenoside C Glc2-Glc OH O-Glc6-Ara(f) OH –
275 V7 Floralquinquenoside D Glc OH O-Glc OH –
276 V8 Ginsenoside III Glc2-Glc OH O-Glc – –
277 V8 Notoginsenoside L17 Glc OH O-Glc6-Xyl – –
278 V8 Notoginsenoside L18 Glc OH O-Glc6-Ara(f) – –
279 V8 Notoginsenoside L19 Glc OH O-Glc6-Ara(f) – –
280 V9 Ginsenoside Rg12 Glc-Glc2 OH OH OH –
281 V10 Ginsenoside L1 Glc OH OH – –
282 V11 Ginsenoside L2 Glc2-Glc OH OH – –
283 V12 Notoginsenosides Ng2 Glc2-Glc OH O-Glc6-Ara(f) – –
284 V12 Notoginsenosides LK1 Glc2-Glc OH O-Glc6-Xyl – –
285 V12 Notoginsenosides LK4 Glc2-Glc2-Xyl OH O-Glc6-Xyl – –
286 V12 Notoginsenosides LK5 Glc2-Glc2-Xyl OH O-Glc6-Ara(p) – –
287 V12 Vinaginsenoside R20 Glc2-Glc OH O-Glc – –
288 V13 Notoginsenosides LK2 Glc2-Glc2-Xyl OH O-Glc-Ara(f) – –
289 V13 Notoginsenosides LK3 Glc2-Glc2-Xyl OH O-Glc – –
290 V13 Notoginsenosides LK15 Glc OH O-Glc6-Xyl – –
291 V14 Notoginsenoside L1 H OH – – –
292 V15 Notoginsenoside L2 Glc2-Glc OH OH – –
293 V16 Notoginsenoside L3 Glc OH – – –
13
294 V17 Sanchirhinoside D Glc2-Glc OH OH – –
295 V18 Koryoginsenoside R2 Glc2-Glc OH O-Glc6-Glc – –
296 V19 3β,6β,12β,20(S)-trihydroxy dammar 24-methyl 1-23-ene-24-carbonyl H OH OH – –
297 V20 3β,12β,20(S),25-tetrahydroxy dammar 23-ene H OH OH – –
298 V20 Quinquenoside L3 Glc OH O-Glc6-Xyl – –
299 V21 27-demethyl-(E,E)-20 (22),23-dien-3β,12β-dihydroxydammar-25-one H OH – – –
300 V22 20(S)-25-ethoxyl-dammarane-3β,12β,20-triol H OH OH CH3 –
301 V22 20(R)-25-ethoxyl-dammarane-3β,12β,20-triol H OH CH3 OH –
302 V23 Quinquenoside L1 Glc2-Glc OH O-Glc – –
303 V24 Isoginsenoside Rh3 Glc OH – – –
304 V25 Floralginsenoside E Glc2-Glc OH OH OH –
305 V25 Floralginsenoside F Glc OH O-Glc OH –
306 V26 Floralginsenoside Kb Glc2-Glc OH O-Glc H –
307 V26 Floralginsenoside KC Glc2-Glc OH O-Glc OH –
308 V27 Bipinnatifidusoside F2 Glc2-Glc OH O-Glc – –
309 V28 Ginsenoside Rz1 Glc2-Glc OH – – –
310 V29 Vinaginsenoside R24 Glc2-Glc OH Glc CH3 –
311 V30 Ginsenoside RT5 Glc OH CH3 – –
Glc: β-D-glucopyranosyl; Gen: gentiobiose; Xyl: β-D-xylopyranosyl; Ara(p): α-D-arabinopyranosyl; Ara(f): α-L-arabinofuranosyl; Rha: α-L-rhamnopyranosyl; —: no substituents.
Table 8
The structure of PPT C17-side chain varied saponins.
L. Liu, et al.
PPT C17-side chain varied
14

Table 8 (continued)
NO. Type R1 R2 R3 R4 R5 R6 Chiral Carbon

L. Liu, et al.
312 W1 OH OH H – – – –
313 W1 OH H H – – – –
314 W1 OH OH H – – – –
315 W1 O-Glc H H – – – –
316 W1 OH O-Glc H – – – –
317 W2 OH O-Glc H H – – –
318 W2 OH O-Glc2-Xyl H H – – –
319 W3 OH O-Glc H H – – –
320 W3 OH O-Glc2-Rha H Glc – – –
321 W3 OH O-Glc2-Rha H H – – –
322 W4 OH O-Glc H Glc – – –
323 W4 OH O-Glc H H – – –
324 W4 OH O-Glc H H – – –
325 W4 OH O-Glc2-Glc H H – – –
326 W4 O-Glc2-Glc H H Glc – – –
327 W4 OH O-Glc H Glc – – –
328 W5 OH OH H OH CH3 – C25:S
329 W5 OH O-Glc2-Rha H OH CH3 – C25:S
330 W5 OH OH H CH3 OH – C25:S
331 W5 OH O-Glc2-Rha H CH3 OH – C25:S
332 W5 OH H H OH CH3 – C25:R
333 W5 OH H H CH3 OH – C25:R
334 W5 OH OH H OH CH3 – C25:R
335 W5 OH OH H CH3 OH – C25:R
336 W5 OH O-Glc2-Rha H CH3 OH – C25:R
337 W5 OH O-Glc2-Rha H OH CH3 – C25:R
15
338 W6 OH O-Glc2-Xyl H OH O-Glc – –
339 W6 O-Glc2-Glc OH H OH O-Glc – –
340 W6 OH OH H OH O-Glc2-Xyl – –
341 W6 O-Glc2-Glc2-Xyl H H OH O-Glc6-Glc – –
342 W6 OH H H OH OH – –
343 W6 OH Glc H OH O-Glc – –
344 W6 OH O-Glc2-Rha H OH O-Glc – –
345 W6 OH O-Glc H OH OH – –
346 W6 OH OH H CH3 O-Glc – –
347 W6 OH OH H OH O-Glc – –
W6 OH OH H OH O-Glc – –
348
349 W6 O-Glc2-Glc OH H OCH3 O-Glc6-Xyl – –
350 W6 OH O-Glc H OOH OH – –
351 W6 O-Glc2-Glc2-Xyl OH H OOH O-Glc6-Glc – –
352 W6 =O OH H OOH OH – –
353 W6 H OH =O OOH OH – –
354 W6 =O H H OOH OH – –
355 W6 OH O-Glc H OOH O-Glc – –
356 W6 OH OH H OOH O-Glc6-Ara(f) – –
358 W6 OH O-Glc2-Rha H OOH OH – –
359 W6 OH OH H OOH O-Glc – –
361 W7 O-Glc2-Glc2-Xyl H H Glc6-Glc – – –
W7 OH O-Glc2-Rha H Glc – – –
362
363 W7 OH Glc H Glc – – –
364 W7 OH OH H Glc – – –

Table 8 (continued)
365 W8 O-Glc2-Glc OH H Glc6-Glc OH – C24:R

L. Liu, et al.
366 W8 OH O-Glc H H OH – C24:R

367 W12 OH O-Glc2-Glc H H – – C24:S
368 W8 OH OH H Glc6-Ara(p) OH – C24:R
369 W8 OH O-Glc H Glc OH – C24:R
370 W8 O-AC-6Glc2-Glc H H Glc OH – C24:R
371 W8 O-Glc2-Glc H H Glc6-Ara(p) OH – C24:R
372 W8 O-Glc2-Glc H H Glc6-Ara(p) OH – C24:R
373 W8 OH O-Glc2-Rha H Glc OH – C24:R
374 W8 OH OH H Glc OH – C24:R
375 W8 OH O-Glc2-Rha H H OH – C24:R
376 W8 OH OH H Glc OH – C24:S
377 W9 OH O-Glc H – – – –
378 W10 OH O-Glc H H – – –
379 W10 OH OH H H – – –
380 W11 OH O-Glc H H – – –
381 W11 OH O-Glc H CH3 – – –
382 W11 O-Glc2-Rha OH H H – – –
W12 OH O-Glc3-Xyl H – – – –
383
384 W12 OH O-Glc2-Rha H – – – –
385 W12 OH OH H – – – –
386 W12 O-Glc2-Glc2-Xyl H H – – – –
387 W13 OH O-Glc H H – – –
388 W13 O-Glc2-Glc H H OCH3 – – –
389 W14 O-Glc2-Glc H H OCH3 – – –
390 W15 OH O-Glc H – – – –
391 W15 OH OH H – – – –
16
392 W16 OH Glc2-Rha H – – – –
393 W16 O-Glc2-Glc2-Xyl H H – – – –
W16 OH OH H – – – –
394
395 W16 O-Glc2-Glc6-AC H H – – – –
396 W16 OH O-Glc2-Rha H – – – –
397 W17 OH O-Glc H – – – –
398 W18 OH O-Glc H – – – –
399 W19 OH O-Glc H – – – –
400 W19 O-Glc OH H – – – –
401 W20 OH O-Glc2-Glc H – – – –
402 W21 O-Glc2-Xyl OH H – – – –
403 W21 O-Glc OH H – – – –
404 W21 OH OH H – – – –
405 W21 OH O-Glc2-Rha H – – – –
406 W21 OH O-Glc Glc – – – –
407 W22 OH O-Glc H – – – –
408 W23 OH O-Glc H OH – – C24:R
409 W23 OH O-Glc2-Glc H OH – – C24:R
410 W23 OH O-Glc2-Rha H O-Glc – – C24:R
411 W23 OH O-Glc2-Rha H O-Glc – – C24:R
412 W23 OH OH H O-Glc – – C24:S
413 W23 OH OH H O-Glc – – C24:S
414 W23 OH Glc H OH – – C24:R
415 W24 OH OH H O-Glc CH3 – –
416 W25 OH O-Glc H O-Glc6-Ara(f) CH3 – –
417 W26 O-Glc2-Glc OH H – – – –
418 W27 OH OH H O–CH2CH3 – – –
419 W27 OH OH H OH – – –

Table 8 (continued)
420 W27 O-Glc H H OH – – –

L. Liu, et al.
W27 OH H H OH – – –
421
422 W27 O-AC OH H OH – – –
423 W27 OH OH AC OH – – –
424 W28 OH OH H O-Glc – – –
425 W29 OH OH H – – – –
426 W30 OH O-Glc H CH3 – – –
427 W30 O-Glc H H CH3 – – –
428 W30 O-Glc2-Glc OH H CH3 – – –
W30 OH O-Glc H OH – – –
429
430 W30 OH O-Glc H OOH – – –
431 W30 OH O-Glc2-Rha H OOH – – –
432 W31 OH O-Glc H CH3 CH3 – C24:S
433 W31 OH O-Glc2-Rha H – O-Glc – C24:R
434 W32 OH O-Glc H OH – – C22:S
435 W33 OH O-Glc H OH – – –
436 W34 OH O-Glc H – – – –
437 W34 OH O-Glc2-Xyl H – – – –
438 W35 OH OH H CH3 OH – –
439 W35 OH O-Glc H OH CH3 – –
440 W35 OH O-Glc2-Xyl H OH CH3 – –
441 W35 OH O-Glc2-Glc H OH CH3 – –
442 W35 OH OH H O-Glc CH3 – –
443 W36 OH OH H – – – C24:S
444 W36 OH OH H – – – C24:R
445 W37 OH OCOCH3 H – – – –
17
446 W38 OH OH H OH CH3 – –
447 W38 OH O-Glc H CH3 OH – –
448 W38 O-Glc H H OH CH3 – –
449 W39 OH H H CH3 OH CH3 –
450 W39 OH H H H OCH3 H –
451 W39 OH OH H H OH CH3 –
452 W39 OH O-Glc2-Rha H H OH CH3 –
453 W40 OH OH H – – – –
454 W40 OH O-Glc H – – – –
455 W41 OH OH H – – – –
456 W42 OH OAC H – – – –
457 W42 AC OH H – – – –
458 W43 O-AC-6Glc2-Glc H H Glc OH – –
459 W43 OH O-Glc2-Rha H Glc OH – –
460 W43 O-Glc2-Glc H H Glc OH – –
461 W43 O-Glc2-Glc H H Glc6-Ara(f) OH – –
462 W44 OH OH H O-Glc – – –
463 W45 OH O-Glc H – – – –
464 W45 OH O-Glc2-Rha H – – – –
Glc: β-D-glucopyranosyl; Xyl: β-D-xylopyranosyl; Ara(p): α-D-arabinopyranosyl; Ara(f): α-L-arabinofuranosyl; Rha: α-L-rhamnopyranosyl; AC: acetyl; —: no substituents.
Table 9
The structure of other saponins.
L. Liu, et al.
18
Table 9 (continued)
L. Liu, et al.
NO. Type Compound R1 R2 R3 R4
465 A Baisanqisaponin A H H X Glc

466 A Baisanqisaponin B H Ara(f) X Glc
467 A Baisanqisaponin C Glc H X H
468 B Pseudo-ginsenoside RT6 O-Glc – – –
19
469 B Pseudoginsengenin R1 OH – – –
470 C Gypenoside L Glc2-Glc H – –
471 C Gypenoside L1 Glc2-Glc H – –
2
472 D 24(R)-Pseudoginsenoside G1 Glc -Glc – – –
2
473 D 24(S)-Pseudoginsenoside G2 Glc -Glc – – –
474 E 3β,4α,12β-trihydroxystigmast-5-en-21-yl octadecan-9′,12′-dienoate R = CO(CH2)7CH]CHCH2CH]CH(CH2)4CH3
475 E stigmast-5-en-3β,4α,12β, 21-tetraol-21-octadec-9′,12′-dienoate R = CO(CH2)7CH]CHCH2(CH2)3CH3
476 F 3β-cis-feruloyloxy-16β-hydroxylup-20 (29)-ene S1'' – – –
477 F 3β-trans-feruloyloxy-16β-hydroxylup-20 (29)-ene S2'' – – –
478 G Notoginsenoside G Glc2-Glc Glc – –
2 6
479 G Yesanchinoside G Glc -Glc Glc -Xyl – –
2 6
480 G Quinquenoside IV Glc -Glc Glc -Glc – –
2 6
481 H Notoginsenoside I Glc -Glc O-Glc -Glc – –
482 H Yesanchinoside I Glc2-Glc O-Glc6-Glc-Xyl – –
483 H Lanost-24-en-3β-ol-3-O-β-D-arabinopyranosyl-(2′→1″)-O-β-D-arabinoside Glc2-Ara(p) CH3 – –
484 I Vina-ginsenoside R3 Glc2-Glc H Glc –
485 J Chikusetsusaponins LT5 Glc H Glc6-Glc –
486 J Chikusetsusaponins LT8 Glc H Glc –
487 J Chikusetsusaponin LN4 Glc6-Xyl H Glc6-Ara –
(p)
488 J 3β,6α-20(S)-6,20-bis(β-D-glucopyranosyloxy)-3-hydroxy dammar-24-en-12-one H Glc Glc –
489 J Chikusetsusaponin FK2 Glc2-Glc Glc – –
490 J Chikusetsusaponin FK3 Xyl-6Glc2-Glc Glc – –
491 K 7β-hydroxyl ginsenoside Rd O-Glc-Glc2 Glc – –
2
492 L 5,6-didehydroginsenoside Rg3 O-Glc-Glc OH – –
493 L 5,6-didehydroginsenoside Rd Glc2-Glc Glc – –
2 6
494 L 5,6-didehydroginsenoside Rb1 Glc -Glc Glc -Glc – –
495 M Notoginsenoside LX Glc Glc6-Ara(f) – –
496 M Notoginsenoside LY H Glc6-Ara(f) – –

Then, a flavonoid glycoside, quercetin-3-O-sophora glycoside was ob

tained from P. notoginseng leaves (Wei et al., 1980). Subsequently, six
flavonoids from the stems and leaves of P. notoginseng were separated
by Zheng et al. (Zheng, 2004). They were identified as kaempferol
(526), quercetin (525), kaempferol-7-O-α-L-rhaamnosioside (529),
kaempferol-3-O-β-D-galactoside, kaempferol 3-O-(2″-β-D-glucopyr
anosyl)-β-D-galactopyranoside (533) and quercetin3-O-(2″-β-D-gluco
pyranosyl)-β-D-galactopyranoside (534). Four other compounds be
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
sides kaempferol (526) and quercetin (525) were isolated from
P. notoginseng for the first time. However, at the moment, there are few
flavonoids from P. notoginseng, most of which exist in the form of fla
C23:R
C23:S
O-Glc
O-Glc
OH
vonols. In addition, some flavonoids were isolated from the flower buds
–
–
–
–
–
–
–
–
–
–
–
–
–
and leaves of P. ginseng. Flavonoids are also important chemical com
ponents in the aerial part of P. ginseng. Three flavonoids, ginsenoside,
O-Glc2-Rha
O-Glc2-Rha
trifolium glycoside and kaempferol were isolated from stem and leaf of
Glc-Ara(p)
Glc-Ara(f)
Glc6-Xyl
Glc6-Xyl
Glc6-Xyl
P. ginseng (Wang et al., 1985). Xu et al. (Xu and Yang, 2016) also iso
Ara(p)
O-Glc
lated two new compounds from P. ginseng buds and identified them as
OH
OH
Xyl
Glc
Glc
H
–
–
–
– kaempferol-3-O-α-L-rhamnoside and kaempferol-3-O-(2,3-di-trans-p-
hydroxy cinnamoyl) -α-L-rhamnoside (536). In recent years, some stu
Glc: β-D-glucopyranosyl; Xyl: β-D-xylopyranosyl; Ara(p): α-D-arabinopyranosyl; Ara(f): α-L-arabinofuranosyl; Rha: α-L-rhamnopyranosyl; —: no substituents. dies have also found that there are flavonoids in the roots of P. quin
Glc2-Rha
Glc2-Glc
quefolius (Zhang et al., 2002a,b).

Glc-Glc
Glc-Glc
Ara(p)
OH
OH
Xyl
Glc
Glc
Glc
Glc
Glc
Glc
Glc
H
–
–
5.4. Polyacetylenes (546–568)
Alkyne hydrocarbons are less distributed in Panax, mainly in the

underground parts of P. notoginseng, P. ginseng, P. quinquefolius and
P. vietnamensis. Under guidance of the growth inhibition experiment of
staphylococcus aureus, Lin et al. analyzed the chemical components of
the fat-soluble parts of P. notoginseng (Lin et al., 2002). Panaxynol (546)
and panaxydol (548) were separated from the petroleum ether fraction
of P. notoginseng for the first time, the yields accounting for 0.01% and
Dammar-24-en-3α,6β,16α,20β-tetraol-3α-D-arabinopyranosyl-6β-D-arabinopyranoside
Dammar-12,24-dien-3α,6β,15α-triol-3α-D-arabinopyranosyl-6β-L-arabinopyranoside
0.033% respectively, which had strong inhibitory effects on staphylo

coccus aureus. Duan et al. used supercritical CO2 extraction method to
6-O-β-D-glucopyranosyl-20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol-3-one
3β,20S-dihydroxy-12β, 23R-epoxydammar-24-ene 3-O-[β-D-glucopyranosyl
obtain P. notoginseng samples with high purity (> 98%) and high yield
3β,6α, 20S-trihydroxy-12β, 23R-epoxydammar-24-ene 6-O-[α-L-rhamnosyl
(0.077%) (Duan et al., 2008). Zhou et al. analyzed the polyacetylene

components in different parts of P. notoginseng by GC-MS (Zhou et al.,
2013). The results showed that the total amount of polyacetylene
6α-hydroxy-22,23,24,25,26,27-hexanordammar-3,12,20-trione
components was higher in the main roots, flowers and rhizomes of

P. notoginseng and lower in stems and leaves. The amount of panaxynol
(1 → 2)-β-D-glucopyranosyl]-20-O-β-D-glucopyranoside
(1 → 2)-β-D-glucopyranosyl]-20-O-β-D-glucopyranoside
(12R,20S,24S)-20,24-;12,24-diepoxy-dammarane-3β-ol
(546) in P. notoginseng flower was higher, but panaxydol (548) could

6-O-β-D-glucopyranosyl-20R-protopanaxadiol-3-one
12β,23(R)-epoxydammara-24-ene-3β,6α,20(S)-triol
hardly be detected. In addition, wei et al. isolated seven polyacetylenes

(20S,22S)-dammar-22,25-epoxy-3β,12β,20-triol
from the underground part of P. vietnamensis, two of which were newly

discovered compounds, namely 10-acetoxy-heptadeca-8(E)-ene-4,6-
diyne-3-ol (561) and heptadeca-l,8(E),10(E)-triene-4,6 diyne-3,12-diol
(573) (Wei, 2001). Two new ones trahydrofuranic polyacetylene gly
cosides, belonging to a novel biogenetically type in nature, panaxfur
12-one-pseudoginsenoside F11
aynes A (563) and B (564) were separated from the root of P. ginseng
(Lee et al., 2009). Five new polyacetylenes (including ginsenoynes A
Pseudoginsenoside-RI2
Notoginsenosides Ng1
Notoginsenoside L14
Notoginsenoside L13
Notoginsenoside Fh8
Notoginsenoside Fh9
(547), ginsenoynes B (549), ginsenoynes C (552), ginsenoynes D (553)

Notoginsenoside P1
Ginsenosides Rh18
and ginsenoynes E (551) were isolated from the hexane extract of the
Ginsenoside La
root of P. ginseng (Hirakura et al., 1991), whose structures were de

termined by spectral and chemical methods. New C17-and C14-poly
acetylenes were isolated from the dried roots of P. quinquefolius by
Fujimoto (Fujimoto et al., 1994).
5.5. Polysaccharides (569–598)
Biologically important polysaccharides have been less widespread

in genus Panax. To date, 30 polysaccharides compounds were isolated
W
M
M
M
M
M
M
from the rhizomes of P. japonicus plants, the roots of P. quinquefolius,

Q
N
N
N
U
V
R
X
Y
T
P
S
Table 9 (continued)
P. notoginseng plants and the flower buds of P. ginseng.
5.6. Fatty acids (599–621)
Lipid is an important component of P. ginseng. Fatty acid compounds

497
498
499
500
501
502
503
504
505
506
507
508
509
510
511
512
513
514
515
516
not only have a wide range of biological activities but also are synthetic
20
precursors of many important biological substances. The fatty acid 2014a,b). Additionally, in a study by Li et al., P. notoginseng poly
component of P. ginseng roots is mainly unsaturated fatty acid and li saccharide was added into the culture medium of H22 hepatoma cells in
noleic acid has the highest content. Lu et al. determined the fatty acid vitro and further administered to neoplasm-bearing mice in vivo. The
content of different processed ginseng products by gas chromatography results showed that P. notoginseng polysaccharide significantly inhibited
(GC) method (Lu et al., 1993). It was found that the linoleic acid (613) the growth of H22 cells and prolonged the survival time of neoplasm-
content of P. ginseng increased up to 62%–65% after heating treatment, bearing mice. The discovery of antineoplastic polysaccharides would
while the relative content of stearic acid was the lowest. The relative broaden the selection of immunotherapeutic drugs for hepatoma (Li
content of stearic acid was less than 1% in P. ginseng and P. quinquefolius et al., 2016). Lee et al. showed that ginseng polysaccharide was a po
root, while P. notoginseng did not contain stearic acid (607) and its oleic tential non-toxic antineoplastic immune activator, which could activate
acid (614) content was close to the sum of the former two. At present, macrophages to produce active nitrogen intermediates, thus subse
24 main fatty acids (including pentadecylic acid (604), palmitic acid quently mediating the tumor killing effects (Lee et al., 1997). Com
(605), stearic acid (607), margaric acid (606), oleic acid (621) and pounds with antineoplastic activity derived from Panax are shown in
linolenic acid (613), etc.) were found in P. ginseng and P. notoginseng Fig. 3.
roots.
6.2. Anti-inflammatory activity
5.7. Other compounds (622–748)
P. ginseng is one of the most widely used alternative drugs to treat
In addition to the above-mentioned compounds, Coumarins, such as inflammation. In recent years, a growing number of studies found that
skimmin (628), apiosylskimmin (629) and daphnin methyl ether (630) ginsenosides had a variety of pharmacological effects against in
were isolated from P. notoginseng plants. On the one hand, phenols, flammatory diseases. Owing to the different chemical structures of
esters, aldehydes and ketones compounds were also separated and ginsenosides, they may have different pharmacological activities and
identified. On the other hand, 14 cyclic dipeptides and five lactamides mechanisms. Ginsenoside Rh2 (20) significantly alleviates in
have been isolated and identified from P. notoginseng plants and flammatory bowel disease in mice induced by dextran sodium sulfate
P. ginseng respectively. Further studies on this research field should be (DSS) (Ye et al., 2014). Ginsenoside F2 is expected to be the alternative
conducted. Eighteen amino acids and 72 trace elements were also iso natural herbal ingredient with low-side-effect to treat the skin in
lated from P. notoginseng and P. trifolius. flammation induced by tetradecanoyl phorbol alcohol acetate (TPA) in
mice (Park et al., 2016). Ginsenoside Rg5 (417) has pharmacological
6. Biological activities effects on anti-neuroinflammation (Xu and Gao, 2017). Ginsenoside Rh1
(100) can effectively stimulate the central nervous system to improve
Modern pharmacological studies showed that genus Panax had an mental acuity and intellectual performance (Tam et al., 2018). In ad
important role in the antineoplastic, anti-inflammatory, hepatorenal dition, the effects of ginsenoside-compound K (G-CK) on T cells in mice
protective, neuroprotective, immunoregulatory, cardioprotective, anti with collagen-induced arthritis showed that G-CK might be a promising
diabetic and anti-hypotensive activities, hemostasis, the activation of drug for the treatment of rheumatoid arthritis (Chen et al., 2018). Dong
blood stasis and etc. The bioactivities of compounds in Panax can be et al. found that the metabolic pathway of ginsenosides (ginsenoside
found in Table 10. Ra1 4, Rb1 13, Rb2 14, Rc 16) in vivo was mainly turned into degly
cosylated ginsenoside (ginsenoside Rd 17) through intestinal microflora
6.1. Antineoplastic activity (Dong et al., 2017). Then it was absorbed into the blood circulation to
exert its effect (Kim et al., 2014). Based on literature review, the anti-
According to the statistics of literature, genus Panax exhibited good inflammatory mechanism of ginsenosides can be roughly attributed to:
antineoplastic activity (as shown in Fig. 2). In 1978, Yun et al. reported (1) exerting antioxidant effect; (2) inhibiting the expression of in
that extract of Radix et Rhizoma Ginseng Rubra inhibited the pro flammatory factors; (3) reducing the phosphorylation and activation of
liferation of dimethylolbutanoic acid (DMBA)-induced neoplasms and MAPK and activation of Protein Kinase B (PKB/Akt); (4) altering in the
prolongated the survival time of mice (Yun and Lee, 2001). Upon 30- intestinal microenvironment. However, a recent study (Han et al.,
year development, the antineoplastic research of ginsenosides has be 2018a) showed that the ethanol extract of ginseng berry calyx (Pg-C-
come a hot spot in P. notoginseng research, with multiple in-depth stu EE) from ginseng plants might have anti-inflammatory properties tar
dies from the metabolism of ginsenosides, antineoplastic mechanisms geting nuclear factor-kB by inhibiting AKT, which suggested that the
and other aspects. development of ginseng berry calyx extract might be beneficial in the
A large number of in vivo and in vitro experiments have proved that treatment of inflammatory diseases.
ginsenosides compounds exhibit significant antineoplastic activities
through some similar pathways. Moreover, the secondary metabolic 6.3. Hepatorenal protection activity
saponins and their saponins produced by ginsenosides under the action
of intestinal bacteria are natural precursors of the antineoplastic effect Chinese herbal medicines have the ability to protect the liver, which
of P. notoginseng (Jin et al., 2006). The main antineoplastic mechanisms have been proved to be the effective anti-inflammatory and anti
can be summarized as follows: (1) cell cycle arrest, induction of oxidant. Panax has the hepatoprotective effects and its mechanism in
apoptosis and inhibition of neoplasm proliferation; (2) inhibitory ef cludes blocking fibrosis, inhibiting tumorigenesis, eliminating viruses
fects on metastasis of cancer cells; (3) activation of the immune system. and inhibiting oxidative damage (Del Prete et al., 2012; Dhiman et al.,
A study revealed that the growth of human cervical cancer cells (HeLa) 2012). Qi et al. first used P. ginseng fruit anthocyanin (GFA), an extract
was inhibited by ginsenoside Rd (17) in a time- and dose-dependent of ginseng fruit, to suppress renal injury induced by cisplatin, demon
manner, with an IC50 value of 150.5 ± 0.8 μg/mL after 48h incubation strating that GFA has a renoprotection effect induced by cisplatin (Qi
(Yang et al., 2006a). Further studies demonstrated that ginsenoside Rb1 et al., 2018). The possible mechanisms include inhibition of cisplatin-
(13) exerted calcium antagonism to reverse the production of cancer induced oxidative stress, reduction of inflammatory response and
cells (Lin et al., 2012). Notoginsenoside Ft1 (36) restrained the cell apoptosis. Ginseng oligopeptides can significantly reduce the levels of
proliferation and induced apoptosis in SH-SY5Y cells through p38 mi tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-
togen-activated protein kinases (MAPK) and extracellular regulated 6 (IL-6) in serum (P < 0.05). Studies have shown that ginseng oligo
protein kinases (ERK)1/2 pathways. It had been shown to have po peptides can protect liver cells by improving alcohol-induced serum
tential therapeutic effects on human neuroblastoma (Gao et al., inflammatory response.
21
Table 10
Biological activities of chemical components isolated from the Panax.
Biological Activities Name Description In vivo/In Reference
vitro
Antineoplastic activity Ginsenoside Rg1 Rg1 (1 mg/L) and Rh1 (100 mg/L) could significantly increase the In vitro Wang (2004)
transcription of dendritic cell IL-12p40 mRNA, which was
consistent with its protein expression
Ginsenoside Rg3 activated caspase-3, caspase-8, and caspase-9 and regulated the In vitro (Park et al., 2014), (Dai
expression of B-cell lymphoma-2 (Bcl-2) and Bax to induce et al., 2019), (Wang et al.,
apoptosis of cancer cells; enhanced the anticancer activity of 2019a,b)
geftinib, making non-small cell lung cancer (NSCLC) cells more
sensitive to geftinib; inhibited autophagic flux and enhancing the
sensitivity of NSCLC cells to icotinib
Ginsenoside Rg2 suppressed the migration and invasion of liver cancer cells by In vivo Sun et al. (2019)
upregulating the protein expression of Abstract Rho Gtpase
activating protein 9 (ARHGAP9)
Ginsenoside Rg5 stimulated the apoptosis of human breast cancer cells; regulated In vitro Kim and Kim (2015)
proteins to block the G0/G1 phase of cell division; inhibited the
increase of breast cancer cells
Ginsenoside Rh1 Rg1 (1 mg/L) and Rh1 (100 mg/L) could significantly increase the In vitro Wang (2004)
transcription of DCIL-12p40 mRNA, which was consistent with its
protein expression
Ginsenoside Rh2 inhibitd the proliferation and induces apoptosis of A375-S2 cell In vitro Hyun-Eui and Lee (1999)
lines cultured in vitro by activating the caspase-8 and caspase-3
signaling pathways
Ginsenoside Rd inhibited the proliferation and promote cell apoptosis of human In vitro (Gu et al., 2019), (Wang
glioma U251 cells; depressed miR-18a-mediated Smad2 et al., 2016), (Yang et al.,
expression regulation; inhibitd HeLa cell proliferation, and 2006b)
induced cell apoptosis through down-regulating Bcl-2 expression;
up-regulated Bax expression; lowered the mitochondrial
transmembrane potential, and activated the caspase-3 pathway
Ginsenoside Re raised p21 level, reduced phosphorylation of cyclinA-cyclin- In vitro Jang et al. (2014)
dependent kinase2 (CDK2), raised S phase arrest
Ginsenoside RK1 inhibited the growth activity of liver cancer cells In vitro Toh et al. (2011)
Ginsenoside RK3 inhibited the growth activity of liver cancer cells In vitro Toh et al. (2011)
Ginsenoside Rb2 inhibited the body pigmentation in the zebrafish in vivo system In vivo Lee et al. (2015)
and reduced melanin contents and tyrosinase activity
Ginsenoside Rh6 the melanogenic inhibitory activity of ginsenoside Rh6 was 23.9% In vivo Lee et al. (2015)
at a concentration of 80 μM and In
vitro
Ginsenoside F4 inhibited Bcl-2 and increased the expression of Bax protein to In vitro Chen et al. (2013)
further promote the apoptosis of JK cells of human
lymphocytoma
Vina-ginsenoside R4 the melanogenic inhibitory activity of vina-ginsenoside R4 was In vivo Lee et al. (2015)
27.8% at a concentration of 81 μM and In
vitro
Vina-ginsenoside R13 the melanogenic inhibitory activity of vina-ginsenoside R13 was In vivo Lee et al. (2015)
35.2% at a concentration of 82 μM and In
vitro
20(S)-dammar-12β,20-dihydroxyl- inhibited the proliferation of hct-8 human colon cancer cell lines In vitro María et al. (2015)
24-ene-3β-succinate with IC50 of 33.5 g/mL
20(S)-dammar-20-hydroxyl-24-ene- inhibited the proliferation of hct-8 human colon cancer cell lines In vitro María et al. (2015)
3β,6α,12β-trisuccinate with IC50 of 38.6 g/mL
Notoginsenoside R1 reduced lung cancer stem cells, reduced epithelial- In vitro (Lee et al., 2017a,b), (Qi
tomesenchymal transition, inhibited the proliferation of HeLa et al., 2012)
cells, up-regulated the gap junction function of cells and
enhanced the cytotoxicity of cisplatin
Notoginsenoside R1 reduced integrin-1 protein, reduced E-selectin, Intercellular In vivo (Wang et al., 2010a,b,c)
adhesion molecule-1 (ICAM-1), enhanced cisplatin cytotoxicity,
enhancement of gap junction's activity, enhancement of gap
junction's activity
25-OCH3-PPD (10, 20, 40 mg/kg) dosedependently increased the latency time In vitro Zhang et al. (2018)
and antinociceptive percentage in hot-plate test
25-OH-PPD (10, 20, 40 mg/kg) dosedependently increased the latency time In vitro Zhang et al. (2018)
and antinociceptive percentage in hot-plate test
Compound K inhibited the enzyme activities of CYP2C9 and CYP3A4 in the In vitro Xiao et al. (2016)
HLMs, The IC50 values were 16.00 μM and 9.83 μM, and Ki values
were 14.92 μM and 11.42 μM for CYP2C9 and CYP3A4,
respectively
Ginsenoside F1 chromatin condensated and increased in the populationof sub-G1 In vivo Tung et al. (2010)
hypodiploid cellsm, IC50 = 23.2 μM
Ginsenoside F2 the cytotoxic effect with IC50 of 50 μg/mL through apoptosis In vivo Shin et al. (2012)
Ginsenoside F5 chromatin condensated and increased in the populationof sub-G1 In vitro (Lee et al., 2017a,b)
Ginsenoside Rp1 decreased the stability of the insulin-like growth-factor-1 In vitro Tung et al. (2010)
receptor (IGF-1R) protein in breast cancer cells
22
Table 10 (continued)

vitro
Floralginsenosides Ta chromatin condensated and increased in the populationof sub-G1 In vitro Kang et al. (2011)
β-elemene inhibited nucleic acid synthesis of tumor cells, induced apoptosis In vitro Tung et al. (2010)
and differentiation of tumor cells, enhanced the immunogenicity
of tumor cells, improved the immune function of tumor cells
Panaxynol inhibited the proliferation of human gastric adenocarcinoma cells In vitro Lu et al. (2016)
in vitro and inhibited the synthesis of DNA, RNA and protein in
cell L1210
Quercetin down-regulated mutated P53 protein, blocked cell cycle, In vitro Lu et al. (2016)
inhibited tyrosine kinase, promoted apoptosis, inhibited heat
shock protein and inhibited the expression of Ras and other
anticancer
Polysaccharide activated CD4 (+) T-cells, raised serum IL-2 In vitro Zhu and He (2004)
Trilinolein modulated phosphoinositide 3-kinase/protein kinase B (PI3K/ In vitro Yoshizaki et al. (2013)
Akt) pathway
Ginseng Pectin SA the maximum inhibition rate of L-929 cell migration was 60% In vitro Yoshizaki et al. (2013)
Ginseng Pectin PGP2a regulated cell cycle and apoptosis to inhibit the proliferation of In vitro Fan et al. (2010)
gastric cancer cells hgc-27
Ginseng Pectin RGAP inhibited the proliferation and metastasis of solid tumors in mice In vitro Li et al. (2014)
Saponin–phospholipid complex decreased the tumor progression on Dimethylolbutanoic acid In vivo Cai et al. (2013)
(DMBA)-induced breast cancer rats and increases the levels of and In
antioxidant enzymes including superoxide dismutase (SOD), vitro
catalase (CAT) and glutathione peroxidase (GPX)
Anti-inflammatory activity Ginsenoside Rb1 enhanced the phagocytic capacity of macrophages for bacteria In vivo Cai et al. (2013)
via activation of the p38/Akt pathway and In
vitro
Ginsenoside Rd dose-dependent inhibited neutrophil kernel factor kappa B (NF- In vitro Xin et al. (2018)
κb) expression with an IC50 value of 3.47, down-regulated the
expression of major mitogen-activated protein kinases (MAPK)
pathway, inhibited the mRNA expressions of inflammatory
factors interleukin-1β (il-1β), il-6, tumor necrosis factor α (tnf-α)
and inducible nitric oxide synthase (iNOS)
Ginsenoside Re down-regulated the expression of MAPK pathway and kappaa B In vitro (Lee, 2014), (Wang, 2011)
pathway, and had an obvious inhibitory effect on the mRNA
expressions of inflammatory factors il-1β, il-6, tnf-α and iNOS
Ginsenoside Rg1 reduced neuronal death in the ischemic region In vivo Wang (2011)
Ginsenoside Rg5 dose-dependent inhibited the expression of NF-κB, with an IC50 In vivo Zheng et al. (2019)
value of 0.61, and inhibited the expression levels of
cyclooxygenase-2(COX-2) and iNOS genes
Ginsenoside Rh1 inhibitd the expression of ifn-gamma-activated Janus kinase/ In vivo (Lee, 2014)
signal transducer and activator of transcription (JAK/STAT) and and In
extracellular regulated protein kinases (ERK) signaling pathways vitro
and their downstream transcription factors NF-κB, interferon
regulatory factor-1 (irf-1) and STAT-1 through iNOS promoters
Ginsenoside Rz1 inhibited the expression of NF-κB, with an IC50 value of 0.63, and In vitro Park et al. (2004)
inhibited the expression levels of cox-2 and iNOS genes to exert
anti-inflammatory effects
Ginsenoside Rf mediated by the brain-derived neurotrophic factor (BDNF)/ In vivo (Lee, 2014)
tropomyosin receptor kinase B (TrkB)/cAMP response element-
binding cAMP response element binding protein (CREB) pathway
Ginsenoside Rk1 inhibited the expression of NF-κB, with an IC50 value of 0.75, and In vitro Qin et al. (2019)
inhibited the expression levels of cox-2 and iNOS genes
Ginsenoside Rp1 inhibited the expression of il-1β in mouse monocytes induced by In vitro (Lee, 2014)
lipopolysaccharide (LPS) by blocking the activation of NF-κB
signaling pathway
Notoginsenoside R1 increased Bcl-2 expression and reduced Bax expression in the In vivo Xiang et al. (2013)
stomach tissues of rats caused by N-methyl-N′-nitro-N-
nitrosoguanidine (MNNG) were eliminated
Vina-ginsenoside R2 be metabolized to ocotillol via presence of recombinant plasmid In vivo Luo et al. (2019)
(PRT4), and the metabolites, particularly ocotillol, may inhibited and In
inflammation by inhibiting the binding of LPS to toll-like vitro
receptors 4 (TLR4) on macrophages
Majonoside R2 be metabolized to ocotillol via PRT4, and the metabolites, In vivo Jeong et al. (2015)
particularly ocotillol, may inhibited inflammation by inhibiting and In
the binding of LPS to TLR4 on macrophages vitro
Compound K downregulated the activities of MAPKs, and NF-κB in LPS-treated In vivo Jeong et al. (2015)
murine peritoneal macrophages and In
vitro
Ginsenoside Rc suppressed TANK-binding kinase (TBK1)/IkB kinase ε/interferon In vitro Joh et al. (2011)
regulatory factor-3 and p38/ATF-2 signaling
Pg-C-EE nuclear-factor-κB-targeted anti-inflammatory properties through In vivo Yu et al. (2017)
suppression of AKT and In
vitro
23

vitro
PQS inhibited apoptosis and inflammation via regulation of In vivo Han et al. (2018b)
endoplasmic, reticulum (ER) stress and the associated and In
inflammatory signaling pathway vitro
Ginseng Pectin Y-5 enhanced the activity of natural killer cells (NK) and phagocytes In vitro Xie et al. (2018)
G-Rh2-B2 reduced expression of TNF-α, IL-6, and IL-1β, and activities of p38 In vitro Cho et al. (2014)
MAPK, and NF-κB
PNFS down-regulated iNOS gene overexpression and thereby decreased In vitro Bi et al. (2012)
NO overproduction via the inhibition of TLR4-mediated MAPK/
NF-κB signaling pathways, but not the PI3K/Akt signaling
pathway
PPQN inhibited TNF-α, IL-1, and IL-6 secretions, followed by NO In vitro Peng et al. (2015)
production with respective values of 40.5%, 41.1%, 34.4%, and
11.1% suppression
Anti-oxidative ability Ginsenoside Rb1 increased the activity of SOD and CAT by more than 10% In vivo Wang et al. (2015)
Ginsenoside Rg1 increased the activity of SOD and CAT by more than 10% In vivo Wang et al. (2015)
Ginsenoside Rf inhibited hypoxia induced-COX-2 expression and cellular In vitro Wang et al. (2015)
migration
Ginsenoside C-Mx increased expression of cytoprotective antioxidants such as heme In vitro Song et al. (2019)
oxygenase-1 (HO-1) and NADPH quinineoxidoreductase-1 (NQO-
1) expression by enhancing the nuclear accumulation of Nuclear
factor erythroid 2-related factor 2 (Nrf2)
Majonoside R2 enhanced gamma-aminobutyric acid (GABAA-ergic) systems in In vitro Liu et al. (2018)
the brain
Ginsenoside Rb1 inhibited the production and accumulation of reactive oxygen In vitro Yobimoto et al. (2000)
species (ROS) in the mitochondria under stress, enhanced
antioxidant enzyme activity, inhibited oxidase activity,
maintained mitochondrial membrane potential stability
CP-1a inhibited on superoxide, hydroxyl and 1,1-diphenyl-2- In vitro Zhou et al. (2019)
picrylhydrazyl (DPPH) radical
CP-2a inhibited on superoxide, hydroxyl and DPPH radical In vitro (Wang et al., 2012a,b)
SLPF EC50 values of reducing activity, DPPH free radical scavenging In vitro (Wang et al., 2012a,b)
activities, the superoxide anion removal ability, and the 2, 2′-
azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) free
radical removal ability are 7.212, 2.893, 2.949, and 0.855 mg/
mL, respectively
Hepatorenal Protection Ginsenoside Rg1 regulated p-erk1/2 and p-jnk pathways, Caspase-3 expression In vitro Dai et al. (2018)
Activity was down-regulated, reduced the expression of oxidation factors
such as GSH and SOD, promoted bcl-2 expression and inhibited
Bax expression in brain tissue, regulated the expression of NO,
activated Nrf2/ho-1 signaling pathway, inhibited tau
phosphorylation
Ginsenoside Rg1 activated Nrf2 signaling pathway, repressed the expression levels In vivo (Wang et al., 2013a,b)
of inflammation-related genes including TNF-α, IL-1β, IL-6, COX-
2, and iNOS
Ginsenoside Rg2 regulated oxidative stress, inflammation, and apoptosis to inhibit In vivo Ning et al. (2018)
cisplatin, induced injury to renal cells and LLC-PK1 cells in rats
Ginsenoside Rg5 regulated oxidative stress, inflammation, and apoptosis to inhibit In vivo Park et al. (2015)
Ginsenoside Rg6 regulated oxidative stress, inflammation, and apoptosis to inhibit In vivo Park et al. (2015)
Ginsenoside Rb1 down-regulated expression of il-1β, upregulated brain-derived In vivo Park et al. (2015)
neurotrophic factor (BDNF) and Caspase3, reduced accumulation
of tau and beta powder, regulated FAS/FASL/P53 protein,
regulated Ca2+ to alleviate glucose (GLU) damage
Ginsenoside Rd down-regulated reduced GLU concentration, Hif-1 expression, In vitro Gao et al. (2010)
suppressed inflammatory factors NF-κB and P38, activated
extracellular regulated protein kinases (ERK) and ark-dependent
signal pathways
Ginsenoside Re reduced melanoma differentiation-associated gene (MDA) and In vitro Waxman and Lynch (2005)
increased SOD expression, decreased acetylcholinesterase
expression, protected the substantia nigra Dopamine (DA),
increased cell DA expression
Notoginsenoside R1 reduced the accumulation of amyloid beta, increased the In vivo (Jin et al., 2006)
expression of choline acetyltransferase, activated Nrf2/ho-1 and In
pathway promotes Nrf2 synthesis, decreased the expression of vitro
TNF-α and il-1β, increased the expression of PPAR gamma protein
Ginsenoside F4 regulated oxidative stress, inflammation, and apoptosis to inhibit In vivo Yang et al. (2016)
cisplatin-induced injury to renal cells and LLC-PK1 cells in rats
Ginsenoside RK3 dose-dependent reduction of cisplatin-induced renal injury in In vitro Park et al. (2015)
LLC-PK1 cells
Ginsenoside Rh4 dose-dependent reduction of cisplatin-induced renal injury in In vitro (Baek et al., 2006)
LLC-PK2 cells
24

vitro
Ginsenoside Rh2 increased expression of Bcl-2 and decreased expression of p53, In vivo (Baek et al., 2006)
Bax, cytochrome c, caspase-8, caspase-9, and caspase-3 in kidney
tissues
Ginsenoside Rg3 reduced NF-κB and iNOS protein expressions In vivo (Qi et al., 2019a,b)
GOP 0.25 g/kg BW dose of ginseng oligopeptide may be more In vivo Kang et al. (2009)
conducive to improve the liver ethanol metabolism enzyme
activity, The serum levels of TNF-α, IL-1β and IL-6 were reduced,
and the serum inflammatory response induced by alcohol was
improved
PQS possessed protective effects in cisplatin-induced Acute Kidney In vivo (Liu et al., 2018a,b,c,d)
Injury (AKI) through suppression of oxidative stress,
inflammation and apoptosis
PNS promoted bcl-2 upregulation, activated the PI3K/Akt pathway, In vitro Ma et al. (2017)
cutted Ang Ⅱ expression, regulated antisense oligonucleotide
(ASO) and icam-1, decreased the expression of H2O2
PNS reduced acute hepatic failure (AHF) acute liver injury, reduced In vivo Si et al. (2016)
mortality and promoted the proliferation and repair of liver cells
Neuroprotective activity Ginsenoside Rb1 inhibitd neuronal apoptosis and increased anti-apoptotic genes In vivo Ren et al. (2007)
and modified the neuroprotective effects of glia-derived
neurotrophic factors in transient cerebral ischemia
Notoginsenoside Rb1 improveed cognitive and sensorimotor deficits by PNS-Rb1, at In vivo Yuan et al. (2007)
least partially, by the modulation of the Akt/mTOR/PTEN
signaling pathway
Ginsenoside Rb2 exerted neuroprotective effects in LPS-stimulated N9 microglial In vitro Yan et al. (2018)
cells by blocking TNF-α production
Ginsenoside Rb3 inhibited the increase of intracellular expansion, the apoptosis of In vitro Wu et al. (2007)
ischemic damaged cells and the activity of aspartic enzyme in the
skin to protect the ischemic brain injury
Ginsenoside Rg1 modulated microglia-mediated cytokines and the related In vivo (Zhu et al., 2010)
upstream mediators, protected neuronal activity and promoted and In
neuroplasticity in particular brain regions associated with vitro
cognition processing
Ginsenoside Rg5 inhibited memory impairment and neuroprotection caused by In vitro (Shi et al., 2019a,b)
alcohol or scopolamine
Ginsenoside Rd reduced NO formation and prostaglandin E2 (PGE2) synthesis In vitro Bao et al. (2005)
and inhibited dendrite loss, cell atrophy, cell body changes and
nerve cell loss in TH (+) cells
Ginsenoside Re increased the expression of bcl-2 protein and bcl-2 mRNA, and In vivo Lorenz et al. (2002)
reduced the expression of bax, baxmRNA, inducible nitric oxide
synthase (INOS) and caspase-3
Ginsenoside Rk1 inhibited memory impairment and neuroprotection caused by In vivo Gando (2010)
alcohol or scopolamine
Pseudoginsenoside-F11 antagonized the memory dysfunction induced by scopolamine In vivo Bao et al. (2005)
Compound K regulated GABAA and gamma-aminobutyric acidB (GABAB) In vitro Konno (1987)
receptors
PNS SH-SY5Y cells exposed to oxygen/glucose deprivation injury by In vivo (Lee et al., 2013a,b)
inhibiting the overexpression of NgR1, RhoA, and Rho-associated and In
coiled-coil protein kinase 2 (ROCK2) vitro
WGP altered the composition and diversity of the gut microbiota in In vivo Shi et al. (2016)
mice with antibiotic-associated diarrhea and promoted the re-
establishment of the microbial environment, thus alleviating the
symptoms of diarrhea
TSPJ upregulated gap-43, a growth-related protein, to improve In vivo Li et al. (2019a,b,c)
learning and memory
Anxiolytic activity Ginsenoside Rg1 be related to the GABA-benzodiazepine-chloride channel receptor In vivo (Wang et al., 2013a,b)
complex
Ginsenoside Rg5 be related to the GABA-benzodiazepine-chloride channel receptor In vivo Cha et al. (2005)
complex
Ginsenoside Rk1 be related to the GABA-benzodiazepine-chloride channel receptor In vivo Cha et al. (2005)
complex
Ginsenoside Rd inhibited the anti-inflammatory effect of LPS by stimulating ht- In vitro Cha et al. (2005)
29 cells to secrete inflammatory factor il-8
Ginsenoside Rb1 reduced Anxiety index, raised Risk assessment, reduced grooming In vivo Lv (2017)
behaviors in electric powered mobile things (EPMT), raised total
number of line crossings of an open field after SPS, reduced SPS-
induced decreasement in hypothalamic neuropeptide Y
expression, raised in locus cerulean tyrosine hydroxylase
expression, reduced expression of BDNF
Ginsenoside Rg3 reduced Anxiolytic effect via γ-aminobutyrate A (GABA A) In vitro Lee et al. (2016)
receptor(s)
Ginsenoside Rh2 antagonized GABA/benzodiazepines In vivo (Lee et al., 2013a,b)
Ginsenoside Rg1 raised both the frequency and duration of open arm entries In vivo Kim et al. (2009)
Ginsenoside Ro raised Both the frequency and duration of open arm entries In vivo Carr et al. (2006)
Pseudoginsenoside-F11 antagonized decreases of DA In vivo Kim et al. (2009)
25

vitro
PNS raised levels of 5-hydroxytryptamine (5-HT), DA and In vitro Wu (2003)

Noradrenaline (NE)
PQS might be related to its effects on certain neuronal systems In vivo (Wang et al., 2011a,b)
Immunoregulatory activity Ginsenoside Rg1 promoted immune factor IL-2, INF-ɤ, IL-12p40 secretion, and In vivo Wei et al. (2007)
enhanced the antitumor immune after chemotherapy, and
reduced cisplatin for the body's immune injury
Ginsenoside Rb1 inhibited TNF-α production in LPS-stimulated RAW264.7 In vitro Wu (2017)
macrophages
Ginsenoside Rb2 inhibited the production of TNF-α in LPS-stimulated In vitro Cho et al. (2001)
RAW264.7 cells and differentiated U937 cells with IC50 values of
27.5 mM and 26.8 mM, respectively
Ginsenoside Rd induced immune responses to T helper 1 (TH1) and T helper 2 In vivo Cho et al. (2001)
(TH2) cytokines
Notoginsenoside L increased the level of immune gloulin in blood plasma In vivo Yang et al. (2007)
Notoginsenoside N increased the level of immune gloulin in blood plasma In vivo
Notoginsenoside R1 combined with aluminum adjuvant, enhanced the immune effect In vivo Chen (2002)
of aluminum adjuvant, reduced its usage, avoided the adverse
reactions caused by high-dose aluminum adjuvant and enhanced
the immunogenicity of HAV antigen
Ginsenoside RT5 increased the production of interlukin-2 (IL-2) cytokine from In vitro Tao et al. (2008)
PMA/Io-activated EL-4 T cells in a dose-dependent manner
20(S)-Ginsenoside Rh2 increased the production of IL-2 cytokine from PMA/Io-activated In vitro Vinh et al. (2019)
EL-4 T cells in a dose-dependent manner
Oleanolic acid β-D-glucopyranosyl increased the production of IL-2 cytokine from PMA/Io-activated In vitro Vinh et al. (2019)
ester EL-4 T cells in a dose-dependent manner
RG-CW-EZ-CP upregulated the phosphorylation of three major MAPKs, In vitro Vinh et al. (2019)
including extracellular signal-regulated kinase, and p38
Ginseng Pectin S-IIA induced human monocytes and thp-1 cells to produce interleukin In vitro Kim et al. (2019)
il-8
Ginseng Pectin SB promoted the secretion of cytokines il-8 and il-2 in human In vitro Sonoda et al. (1998)
monocytes thp-1 and mouse spleen cells at low concentrations
Ginseng Pectin SB inhibited the secretion of cytokines il-8 and il-3 by human In vitro (Tian et al., 2011a,b)
monocyte thp-1 and mouse spleen cells in high concentration
PNS enhanced the humoral and cellular immune responses to In vitro (Tian et al., 2011a,b)
ovalbumin (OVA) in mice when given together with OVA
Improve microcirculation Ginsenoside Rg1 inhibited the adhesion of white blood cells to endothelial cells In vivo Qin et al. (2006)
activity and the degranulation of mast cells, and Rg1 and R1 inhibited the
production of Lps-induced granulocytes H2O2 at 1.0 mg/mL
Ginsenoside Rb1 inhibited the adhesion between white blood cells and endothelial In vivo Sun et al. (2007)
cells and the degranulation of mast cells Rb1 (1.0 mg/mL) and R1
(0.2 mg/mL) significantly inhibited the expression of Lps-induced
granulocytes CD11b and CD18
Notoginsenoside R1 inhibited the adhesion between white blood cells and endothelial In vivo Sun et al. (2007)
cells and the degranulation of mast cells Rb1 (1.0 mg/mL) and R1
(0.2 mg/mL) significantly inhibited the expression of Lps-induced
granulocytes CD11b and CD18
Cardioprotective activity Ginsenoside Rb1 reduced apoptosis of cardiomyocytes caused by ischemia In vivo Sun et al. (2007)
reperfusion injury
Ginsenoside Rb3 protected myocardial function during ischemia and inhibited In vivo Liu and Liu (2002)
proliferation of vascular smooth muscle cells, Calcium channels
have a blocking effect
Ginsenoside Rc calcium channels have a blocking effect In vitro (Wang et al., 2010a,b,c),
(Wang et al., 2010a,b,c)
Ginsenoside Rd inhibited the receptor regulation of vascular smooth muscle cells, In vitro Sun et al. (1994)
ameliorated isoproterenol (ISO)-induced cardiotoxicity in rats via
upregulation of the activities of antioxidants, and suppression of
inflammatory and apoptotic biomarkers
Ginsenoside Rd improved cardiac dysfunction and remodeling induced by In vivo (Guan et al., 2006), (Sun
pressure overload and In et al., 2019a,b)
vitro
Ginsenoside Rd ameliorates ISO-induced cardiotoxicity in rats via upregulation of In vivo (Zhang et al., 2019a,b)
the activities of antioxidants, and suppression of inflammatory
and apoptotic biomarkers
Ginsenoside Re reduced apoptosis of cardiomyocytes caused by ischemia In vivo (Sun et al., 2019a,b)
reperfusion injury, attenuated isoproterenol-induced myocardial
ischemic injury by regulating the antioxidation function in
cardiomyocytes, improved isoproterenol-induced myocardial
fbrosis and heart failure by regulation of the transforming growth
factor beta 1 (TGF-1)/Smad3 pathway
Ginsenoside CK reduced myocardial ischemia reperfusion in mice with In vivo (Liu and Liu, 2002), (Wang
myocardial infarction area and Ca2+ induced mitochondrial et al., 2018), (Wang et al.,
distention 2019)
26

vitro
Ginsenoside RK3 inhibited protein kinase B/Nuclear respiratory factor-2/heme In vivo Tsutsumi et al. (2011)
oxygenase-1 (AKT/nrf-2/ho-1) and MAPK pathways, and
prevented the injury and apoptosis of H9C2 cells
Ginsenoside Rh1 inhibited the activities of L and T Ca2+ channels, reducing their In vitro Sun et al. (2013)
opening probability and opening time
Notoginsenoside R1 inhibited TNF-α-induced Plasminogen activator inhibitor-1(PAI- In vitro Zhao et al. (2011)
1) overexpression in HASMCs by suppressing ERK and PKB
signaling pathways
Notoinsenoside Rg1 attenuated pulmonary vasoconstriction which may lead to HHPV In vitro Zhang and Wang (2006)
through reducing the expression of ERK1/2.
PQS inhibited excessive endoplasmic reticulum stress (ERS) In vivo Zhang et al. (2016)
and In
vitro
PNS activated PI3K/Akt signaling pathway In vivo (Wang et al., 2012a,b)
and In
vitro
PNS inhibited the changes of NF-κB, reduced the expression of In vivo Chen et al. (2011)
intercellular adhesion factor and neutrophil infiltration
PNS increased miR-29c expression and decreased the expression of In vivo Tang et al. (2002)
miR-29c target genes in ISO-challenged mouse hearts
PNS reduced the duration of arrhythmias induced by aconitine, BaCl2, In vivo Liu et al. (2017)
and Cacl2-Ach
Antiobesit ability Chikusetsusaponins inhibited pancreatic lipase activity and delaied intestinal dietary In vivo Leng et al. (2001)
III absorption
Chikusetsusaponins IV inhibited pancreatic lipase activity and delaied intestinal dietary In vivo Han et al. (2005)
absorption
28-deglucosyl-chikusetsusaponins inhibited pancreatic lipase activity and delaied intestinal dietary In vivo Han et al. (2005)
IV absorption
28-deglucosyl-chikusetsusaponins V inhibited pancreatic lipase activity and delaied intestinal dietary In vivo Han et al. (2005)
absorption
Ginsenoside Rh2 induced carnitine palmitoyltransferase-1 (CPT-1) and uncoupling In vivo Han et al. (2005)
protein-2 (UCP-2) and In
vitro
Ginsenoside Rc inhibited pancreatic lipase activity by 100% at 0.5 mg/mL In vitro Hwang et al. (2007)
Ginsenoside Rb1 inhibited pancreatic lipase activity by 96% at 0.5 mg/mL In vitro (Zhang et al., 2002a,b)
Ginsenoside Rb2 attenuated insulin resistance in 3T3-L1 adipocytes, reduces fat In vivo (Zhang et al., 2002a,b)
mass, and improves insulin sensitivity in high fat diet-obesity
mice
Notoginsenoside Fe through the activation of energysensing neurons in the In vivo Dai et al. (2018)
hypothalamus and In
vitro
Ginsenoside Rh1 inhibited adipocyte differentiation and inflammation In vitro Li et al. (2019a,b,c)
Ginsenoside Rg1 induced AMPK activation, inhibiting lipogenesis, and decreasing In vivo Gu et al. (2013)
intracellular lipid content, adipocyte size, and adipose weight
PNS inhibited pancreatic lipase activity by 35.2% at 0.5 mg/mL In vitro (Liu et al., 2018a,b,c,d)
PNS raised transcriptional activation of the liver X receptors (LXR) α In vivo (Zhang et al., 2002a,b)
gene promoter, reduced NF-κB DNA binding activity and In
vitro
PQS inhibited pancreatic lipase activity by 90% at 0.5 mg/mL In vitro Fan et al. (2012)
Ginsenoside Rb1 promoted adipocyte differentiation, inhibited basal lipolysis, In vitro (Zhang et al., 2002a,b)
decreased fasting blood glucose level (FBGL), improved GT
Ginsenoside Rb1 improved glucose tolerance (GT), decreased body weight In vivo (Shang et al., 2007), (Park,
incremental percentage and FBGL 2008)
Ginsenoside Re improved GT, decreased body weight incremental percentage and In vivo Yang et al. (2010)
FBGL, decreased gluconeogenesis, activated AMPK, inhibitd
glycogenolysis, decreased lipogenesis, decreased insulin
resistance
Ginsenoside Rc induced Reactive oxygen species (ROS) generation, activate In vitro Yang et al. (2010)
AMPK and p38 MAPK
Ginsenoside Rg1 protected retinal pigment epithelium (ARPE)-19 cells against HG- In vitro (Lee et al., 2010a,b)
induced injury through up-regulating miR-26a, along with
inhibition of the ERK and Wnt/β-catenin pathways, relieved the
insulin-induced insulin resistance in HepG2 cells, decreased
gluconeogenesis, activated AMPK, enhanced of insulin binding in
liver membranes
Ginsenoside M showed dose-dependent hypoglycemic actions 7 h after injection In vivo (Shi et al., 2019a,b), (Park,
and still exhibited significant actions even after 24 h. Z.p. dosing 2008), (Tchilian, 1991)
of the main glycan, panaxan N
Ginsenoside N showed dose-dependent hypoglycemic actions 7 h after injection In vivo Konno (1987)
and still exhibited significant actions even after 24 h. Z.p. dosing
Ginsenoside O showed dose-dependent hypoglycemic actions 7 h after injection In vivo Konno (1987)
27

vitro
Ginsenoside P showed dose-dependent hypoglycemic actions 7 h after injection In vivo Konno (1987)
Compound K protected islet B cells In vivo Konno (1987)
PNS improved glucose homeostasis, increased insulin sensitivity, In vivo Han et al. (2007)
improved leptin sensitivity, improved glucose uptake, improved
insulin-and leptin sensitivity
AF in vitro, AF and AFG inhibited the IC50 of intestinal α-glycosidase In vitro Yang et al. (2010)
and α-amylase in rats by 6.40 and 6.20 mM, and in vivo, the IC50 and In
inhibited pancreatic α-amylase by 36.30 and 37.60 mM vivo
AFG in vitro, AF and AFG inhibited the IC50 of intestinal α-glycosidase In vitro Ha et al. (2011)
and α-amylase in rats by 6.40 and 6.20 mM, and in vivo, the IC50 and In
inhibited pancreatic α-amylase by 36.30 and 37.60 mM vivo
PA reduced blood glucose and improve glucose tolerance in patients In vivo Ha et al. (2011)
with 2 diabetes mellitus
TGCG lowered the fasting blood glucose levels in ob/ob mice In vivo Yoshinari and Igarashi
(153 ± 16 mg/dL vs 203 ± 9.8 mg/dL, P < 0.01, compared to (2011)
vehicle-treated group)
Hemostatic activity Dencichine (β-N-oxalyl-L-α,β- promoted platelet aggregation induced by low dose trap and ADP In vivo (Xie et al., 2005)
diaminopropionic acid)
Notoginsenoside Ft1 activated the P2Y12 receptor signaling pathway to promote adp- In vitro (Li et al., 2018b)
induced platelet aggregation
PNS lower bleeding times (9.60 ± 1.50 min) than the control group In vivo (Gao et al., 2014a,b)
(19.23 ± 4.09 min, P < 0.001) or the placebo group
(15.18 ± 2.24 min, P < 0.001)
Antithrombotic activity Ginsenoside Rb1 promoted the proliferation of erythropoietic progenitor cells In vitro (White et al., 2000)
Ginsenoside Rb1 extended the time from the onset of irradiation to the onset of the In vivo Zheng et al. (2003a)
clot and reduced the size of the clot
Ginsenoside Rb3 inhibitd platelet activation and aggregation In vitro Fang et al. (2008)
Ginsenoside Rg1 extended the time from the onset of irradiation to the onset of the In vivo Cui et al. (2006)
clot and reduced the size of the clot
Ginsenoside Rg1 promoted the proliferation of human bone marrow granulocytes, In vitro Fang et al. (2008)
inhibitd platelet receptor-activated calcium channels and lowers
platelets
Ginsenoside Rg2 increased the content of cAMP in platelets In vivo (Zheng et al., 2003a), (Liu
et al., 2007)
20(S)-ginsenoside Rg3 the affinity of fibrinogen and fibronectin with αIIb/β3 was In vitro Zhang and Chen (1984)
inhibited by G-Rg3 via cyclic AMP-dependent vasodilator-
stimulated phosphoprotein (VASP) Ser157 phosphorylation
Ginsenoside Rk1 inhibited cyclooxygenase activity to reduce thromboxane B 2 In vitro Kwon (2018)
(TXB2) levels and reduce 12-HETE levels
Chikusetsusaponins Iva With Gp Ⅱ b/Ⅲ a receptor inhibition activity In vitro (Lee et al., 2010a,b)
Araloside A With Gp Ⅱ b/Ⅲ a receptor inhibition activity In vitro Nguyen et al. (2011)
Chikusetsusaponins Ib With Gp Ⅱ b/Ⅲ a receptor inhibition activity In vitro Nguyen et al. (2011)
Ginsenoside Re proliferated hematopoietic progenitor cells In vitro Nguyen et al. (2011)
Ginsenoside Ro inhibited the formation of 1,2-hydroxy-5,8,10-heptadecatrienoic In vitro Zheng et al. (2003b)
acid and thromboxane B2
Ginsenoside R1 proliferated hematopoietic progenitor cells In vitro Kuo et al. (1990)
Notoginsenoside R1 improved microcirculation and moderately prolonged In vivo Zheng et al. (2003b)
coagulation time
Notoginsenoside Rd improved microcirculation and moderately prolonged In vivo (Fang et al., 2008), (Liu
coagulation time et al., 2007)
Notoginsenoside Rh1 binded to human platelets In vitro Liu et al. (2007)
Notoginsenoside Rf1 binded to human platelets In vitro Liu et al. (2012)
PNS increased coronary heart disease patients serum NO, endothelin In vitro Liu et al. (2012)
levels drop, reduced vascular endothelin Ⅱ (Ang Ⅱ) induced
endothelial cell apoptosis rate and Fas and the expression of Bcl-2
PJSM accelerated the recovery of red blood cells (RBC), white blood In vitro Zheng et al. (2003b)
cells (WBC) and haemoglobin (HGB) levels in blood deficiency
model mice
PJPS accelerated the recovery of RBC, WBC and HGB levels in blood In vitro Zhang (2015)
deficiency model mice
Ocotillol inhibited the formation of arteriovenous bypass thrombosis in In vitro Zhang (2015)
rats
Vidarabine binded to human platelets In vitro María et al. (2015)
Guanosine binded to human platelets In vitro Liu et al. (2012)
Anti-atherosclerosis activity Ginsenoside Rd inhibited the formation of foam cells in vitro and reduced In vivo Liu et al. (2012)
atherosclerotic plaques
Ginsenoside Rh2 reduced serum il-6 level and inhibited the expression of timp-1 In vivo Li et al. (2011)
and Vascular endothelial growth factor (VEGF) in aorta of rats
PNS inhibited the effect of high-fat animal serum on smooth muscle In vivo Zhang (2015)
cell (SMCs) and significantly inhibited the occurrence of
atherosclerosis and the formation of aortic intima plaque in
experimental animals
28

vitro
PNS maintained vascular smooth muscle cell (VSMCs) contractile In vitro Zhang (2015)
phenotype
PNS inhibited NF-κB DNA binding activity and reduced secretion of In vivo Liu et al. (2015)
IL-6 and MCP-1 in LPS-stimulated THP-1 macrophages and In
vitro
Haemolytic Activity Notoginsenoside K increased the concanavalin A (Con A)-, lipopolysaccharide (LPS)-, In vivo Fan et al. (2012)
and OVA-induced splenocyte proliferation in OVA-immunized
mice (P < 0.05, P < 0.01, or P < 0.001)
Pseudoginsenoside-F11 activated cholinergic transmission to antagonize morphine- In vitro Qin et al. (2006)
induced memory deficits, activated dopaminergic transmission to
inhibit morphine-induced conditioned place preference,
regulated adenylyl cyclase activity toeliminate morphine-induced
tolerance development.
PNS haemolytic percents of PNS-treated red blood cell were 11.6% In vitro (Han et al., 2018a,b)
and 3.6% at concentrations of 500 and 250 mg/L, respectively
Autotoxicity Ginsenoside Rg1 excessive accumulation of reactive oxygen species (ROS) can be In vitro Qin et al. (2006)
induced to cause oxidative damage to cells, lead to root tip cell
necrosis, and finally inhibit root growth
Ginsenoside Rh2 selectively inhibited the activity of osteoclast growth factor In vitro (Luo et al., 2019a,b)
secreted by RAW264.7 macrophages in vitro
Cytotoxicity activity Panaxytriol inhibitd cellular respiration and disrupts cellular energy balance In vitro Liu et al. (2009)
in Breast M25-SE
Allelopathic inhibitory Ginsenoside Rg1 MSI3 = −0.374, which inhibited seedling height, principal root In vitro Matsunaga et al. (1995)
activity length, soluble protein content, soluble sugar content and CAT
activity
Ginsenoside R1 MSI3-0.221, which inhibited seedling height, principal root In vitro Ma et al. (2016)
length, soluble protein content, soluble sugar content and CAT
activity
PNS MSI3 = −0.426, which inhibited seedling height, principal root In vitro Ma et al. (2016)
length, soluble protein content, soluble sugar content and CAT
activity
Anti-muscular atrophy Ginsenoside Rg1 inhibited the decrease of C2C12 cell activity and apoptosis In vitro Ma et al. (2016)
activity induced by serum-free culture, inhibited the expression of two
muscle-specific ubiquitin ligase E3
Ginsenoside Rb1 increased the expression of bcl-2 protein, decreased the In vitro Li (2016)
expression of Bax protein, and increased the ratio of bcl-2/Bax
reduces the apoptosis of hypoxia-induced nerve cells
Ginsenoside Rb2 upregulated myotube growth and myogenic differentiation In vivo Nie et al. (2004)
through activating Akt/mammalian target of rapamycin signaling and In
and inducing myogenic conversion of fibroblasts vitro
20(S)-ginsenoside Rg3 inhibited growth and survival of GBC cells via activation of the In vivo Go et al. (2019)
p53 pathway and In
vitro
Ginsenoside Rg3 attenuated TNF-α-induced NPCs impairment via blocking the NF- In vitro Dong et al. (2015)
κB signaling pathway
PNS attenuated oxidative damage through oxidative stress- and In vivo Chen et al. (2019)
mitochondrial function-related signaling pathways
PQS increased cardiomyocyte viability and decreased cardiomyocyte In vivo Zhou et al. (2018)
apoptosis induced by TG and In
vitro
Anti-bacterial activity Oleanolic acid displayed 98.75% and 97.26% feeding-deterrence at 3000 ppm In vivo (Ma et al., 2015)
concentration
Antiviral activity Ginsenoside Rb2 potentiated nonspecific resistance against severe infection of In vivo Shukla (1997)
reovirus (RV) in newborn mice
20(S)-Ginsenoside Rg3 potentiated nonspecific resistance against severe infection of RV In vivo Yang et al. (2018)
in newborn mice
Ginsenoside Rg3 promoted CO cell proliferation, promotes CO cell immune In vitro Yang et al. (2018)
activities, and thereby enhances the resistance of CO to grass carp
tissues after reovirus (GCRV) infection
Anti-osteoporosis activity LPNS promoted the differentiation of bone marrow mesenchymal stem In vivo Dai (2018)
cells and mononuclear cells into osteoblasts and osteoclasts, and In
respectively, but had no effect on osteoclast activation vitro
Anti - proliferation activity Ginsenoside Re IC50 = 0.489 mg/mL, The highest cell proliferation inhibition In vitro Du et al. (2015)
rates were 71% at 1 mg/mL
Ginsenoside Rg1 IC50 = 0.653 mg/mL, The highest cell proliferation inhibition In vitro Yao et al. (2014)
rates were 59.4% at 1 mg/mL
Ginsenoside Rb1 IC50 = 0.553 mg/mL, The highest cell proliferation inhibition In vitro Yao et al. (2014)
rates were 68% at 1 mg/mL
Anti-allergic activity Ginsenoside Rf inhibited the release of β-aminohexidase, IC50 = 0.08 mmo/L In vivo Yao et al. (2014)
Ginsenoside Rh2 inhibited the release of β-aminohexidase, IC50 = 0.03 mmo/L In vivo Bae et al. (2006)
Ginsenoside Rg3 inhibited the release of β-aminohexidase In vivo Bae et al. (2006)
Ginsenoside Re reduced blood glucose, total cholesterol and triglyceride levels In vivo Bae et al. (2006)
PNS caused a decrease in platelet activator, Calcium channel blockers, In vitro Cho et al. (2006)
Blocked the norepinephrine induced internal flow
29

vitro
Endothelial cell protective Ginsenoside Rb1 inhibited TGF-β related signal transduction and protected human In vitro Chen et al. (2004)
activity umbilical vein endothelial cells (HUVECs), with Rb1 = 80 mg/L
Anti-cell migration activity Ginseng Pectin WGPA inhibition was correlated with GalA content (HG domain) and In vitro Xie et al. (2008)
Rha content (rg-i domain)
Anti-apoptosis activity Ginsenoside Rg2 down-regulated the expression of pro-apoptotic factors BAX and In vivo (Fan et al., 2010)
P53
Anti-radiation activity Notoginsenoside R1 R1 with a mass concentration of more than 50 μm g/mL In vitro Zhang et al. (2008)
decreased cell proliferation activity, hydroxyproline and total
collagen secretion, and increased mmp-1 protein secretion in
fibroblasts
Ginseng Pectin APG blocked the p53-dependent pathway and the mitochondrial/ In vivo Xie et al. (2011)
caspase pathway, and finally protected the small intestinal crypt and In
cells and prevented villi injury vitro
Myelosuppressive activity Compound K controlled apoptosis and promote cells enter the normal cell cycle In vitro Park et al. (2011)
by bcl-2/bax signaling pathway and/MAP kinase–ERK kinase/
extracellular-signal-regulated kinase (MEK/ERK) signaling
pathway
Anti-acne activity RGEF oxidized sebum contents and redness of the skin were reduced, In vivo Han et al. (2019)
and symptoms of the early to middle stage of acne were
effectively improved
Gastrointestinal protective PNS increased vascular endothelial growth factor A (VEGFA) In vitro Hou et al. (2019)
activity expression
Anti-complement activity Ginsenoside Re ginseng saponins imposed their effects on complements C1q, C2, In vitro Zhu et al. (2018)
C3, C4, and C5, however, maybe not C9
Ginsenoside Rf ginseng saponins imposed their effects on complements C1q, C2, In vitro Gao et al. (2013)
Ginsenoside Rg1 ginseng saponins imposed their effects on complements C1q, C2, In vitro Gao et al. (2013)
Anti-complement activity Ginsenoside Rb3 ginseng saponins imposed their effects on complements C1q, C2, In vitro Gao et al. (2013)
Notoginseng R4 ginseng saponins imposed their effects on complements C1q, C2, In vitro Gao et al. (2013)
Acidic polysaccharides GL-NIa through the alternative complement pathway In vitro Gao et al. (2013)
Acidic polysaccharides GL-NIb through the alternative complement pathway In vitro Gao et al. (2013)
Acidic polysaccharides GL-AIa through the alternative complement pathway In vitro Gao et al. (1991)
Acidic polysaccharides GL-AIb through the alternative complement pathway In vitro Gao et al. (1991)
Anti-hypertensive activity Ginsenoside Rb1 increased endothelial-dependent vessel dilatation through the In vivo Gao et al. (1991)
activation of NO by modulating the PI3K/Akt/eNOS pathway and and In
L-arginine transport in endothelial cells vitro
Ginsenoside Rg1 increased endothelial-dependent vessel dilatation through the In vivo Pan et al. (2012)
activation of NO by modulating the PI3K/Akt/eNOS pathway and and In
L-arginine transport in endothelial cells vitro
Anti-hepatitic Activity Ginsenoside Ro inhibited GalN- and CC14-induced cytotoxicity in primary In vitro Pan et al. (2012)
cultured rat hepatocytes
Myelosuppressive activity Ginsenoside Re regulated the levels of cytokines, promoting cells enter the In vivo Matsuda et al. (1991)
normal cell cycle, regulated the balance of bcl-2/bax, and and In
inhibited the expression of caspase-3 vitro
Ginsenoside RK3 regulated the levels of cytokines, promoted cells enter the normal In vivo (Han et al., 2018a,b)
cell cycle, regulated the balance of bcl-2/bax, and inhibited the and In
expression of caspase-3 vitro
PNS promoted DO and mediated by TGF-β1 signaling pathway In vivo (Han et al., 2018a,b)
and In
vitro
PNS inhibited the accumulation of collagen and then inhibit In vivo Guo et al. (2017)
hypertrophic scarring through reducing CTGF expression and
increasing MMP1 expression
Analgesic activity Ginsenoside Rc suppressed pain induced by chemical stimulation through the In vivo Zhi (2017)
non-opioid system
Ginsenoside Rd suppressed pain induced by chemical stimulation through the In vivo (Lee et al., 2015a,b,c)
non-opioid system
Ginsenoside Re suppressed pain induced by chemical stimulation through the In vivo (Lee et al., 2015a,b,c)
non-opioid system
Sedation activity Ginsenoside Rb1 reduced the amount of synaptic glutamate inhibits the central In vitro (Lee et al., 2015a,b,c)
nervous system
Notoginsenoside R1 R1 of 100 mg kg−1 reduced the voluntary activity induced by In vivo Cicero et al. (2003)
caffeine in mice
PNS reduced the amount of synaptic glutamate inhibits the central In vitro Cui et al. (2009)
nervous system
Anti-depressant activity Ginsenoside Rb1 mediated by central neurotransmitters of serotonergic, In vivo (Ma et al., 1999)
noradrenergic and dopaminergic systems, antagonized by 5-
HT2AR antagonists (Ritanerin)
Ginsenoside Rg1 reduced CMS-induced increasement of corticosterone levels in In vivo Wang et al. (2017)
serum, increased Chronic unpredictable mild stress (CUMS)
-induced CREB phosphorylation in the amygdala of the brain
30

vitro
Ginsenoside Rg3 reduced IL-6 and TNF-α in plasma and the expression of In vivo Liu et al. (2016)
indoleamine 2,3-dioxygenase (IDO) in brain
Ginsenoside Rg5 increased expression of brain neurotrophic derived factor (BNDF) In vivo Kang et al. (2017)
Ginsenoside Rh2 reduced turnover of tryptophan and 5-HT in hippocampal tissue In vivo Xu and Gao (2017)
Ginsenoside K the antidepressant effects of Rb1 and the metabolite ginsenoside In vivo You et al. (2017)
K may be antagonized by 5-HT2AR antagonists (Ritanerin),
indicating that Rb1 has a similar 5-HT transmitter activation
effect
Ginsenoside Re regulated the secretion of corticosterone from the Hypothalamic- In vivo Carr et al. (2006)
pituitary-adrenal (HPA) axis
Ginseng Pectin WGPA WGPA of 100 mg/kg can significantly increase the social In vivo Lee (2018)
interaction of mice and reduce the aggressive behavior of mice
PNS reduced Immobility time in forced swim test (FST) and tail In vivo Wang et al. (2014)
suspension test (TST), increased sucrose intake in sucrose and In
preference test vitro
PNS raised level of animal activity, modulated of brain monoamine In vivo (Wang et al., 2016a,b,c,d)
neurotransmitters and intracellular Ca2+ concentration
GTS reduced mRNA of IL-1β, IL-6, TNF-α and IDO In vivo Carr et al. (2006)
Anti-aging activity Ginsenoside Rb1 increased the activity of catalase and glutathione peroxidase In vivo Kang et al. (2017)
Compound K CK did not regulate tyrosinase activity and melanin secretion, but In vitro Dai et al. (2018)
increased melanin content in B16F10 cells was observed
Pg-C-EE suppressed ROS generation induced by H2O2 and undergoing In vivo Kim et al. (2018)
photo therapy (UVB)
Anti-fatigue activity (24R)-Pseudo Ginsenoside HQ upregulated the innate and adaptive immune response in In vitro Lee (2018)
cyclophosphamide (CTX), induced-immunocompromised mice
(24S)-Pseudo Ginsenoside HQ upregulated the innate and adaptive immune response in In vitro (Qi et al., 2019a,b)
cyclophosphamide (CTX), induced-immunocompromised mice
Ginsenoside Rg1 increased SOD activity, mitochondrial membrane potential and In vivo (Qi et al., 2019a,b)
free calcium content in rat skeletal muscle, but decreased MDA
content
Ginsenoside Rb1 the intracellular calcium overload was reduced by inhibiting the In vivo Yichong et al. (2010)
intracellular calcium flow to protect ischemic nerve cells, and the
protective effect was concentration-dependent, reaching the
maximum at 60 mol/L
Ginsenoside Rb3 the intracellular calcium overload was reduced by inhibiting the In vivo Zhang et al. (2005)
intracellular calcium flow to protect ischemic nerve cells, and the
protective effect was concentration-dependent, reaching the
maximum at 60 mol/L
WGP the FST-induced reduction in glucose and glutathione peroxidase In vivo Zhang et al. (2004)
and increase in creatine phosphokinase, lactic dehydrogenase
and malondialdehyde levels
Ginseng Pectin WGPA have therapeutic effects on chronic fatigue syndrome In vivo (Wang et al., 2010a,b,c)
Antifibrotic activity Ginsenoside Rd inhibited CD36 protein expression and reduced lipid intake to In vitro Wang et al. (2014)
inhibit activated HSCs proliferation and COL1A1 protein
expression
Ginsenoside Rg1 down-regulated the expression of Platelet-derived growth facto In vivo (Li et al., 2016)
(PDGF) receptor-β by reducing the NF-κB activity and In
vitro
Ginsenoside Rg1 restrained the process of EMT maybe via suppressing the In vitro Geng et al. (2010)
expression of P-ERK1/2
Ginsenoside Rg1 reduced the deposition of collagen in liver tissue and improved In vivo Xie et al. (2009)
the degree of liver fibrosis
PNS reduced the deposition of collagen in liver tissue and improved In vivo Dong et al. (2012)
the degree of liver fibrosis, inhibited on the NF-κB signaling
pathway
PNS alleviated liver damage and reduced the formation of fibrous In vitro (Zhang et al., 2018a,b)
septa
Anti-vascular aging activity Ginsenoside Rg1 reduced p16INK4a/Rb and p53-p21Cip1/Waf1 signaling In vitro Hui et al. (2016)
pathways
Anti-vascular aging activity Notoginsenoside R1 via the activation of the Vascular endothelial growth factor In vivo (Gao et al., 2014a,b)
(VEGF)-KDR/Flk-1 and phosphatidylinositol-3 kinase (PI3K)-Akt- and In
eNOS signaling pathways vitro
PNS reduced expression of Proliferating cell nuclear antigen (PCNA), In vivo (Gao et al., 2014a,b)
reduced cyclin E, cyclin D1, fibronect, and MMP-9
PNS reduced cell cycle-related factors and ERK signal transduction, In vitro Wu et al. (2010)
raised p53, Bax, and caspase-3 expressions, reduced Bcl-2
expression, protected ECs and in inhibiting platelet adhesion to
injured ECs, and the regulation of COX pathway in both ECs and
platelets
PNS VEGF-KDR/Flk-1and PI3K-Akt-eNOS signaling pathways In vivo (Hang, 2012), (Xu et al.,
and In 2011), (Wang et al.,
vitro 2016a,b,c,d)
31

vitro
(Hong and Wang, 2009)
PPD: Protopanaxadiol; PPT: protopanaxatriol; PNS: Panax notoginseng saponin; PQS: Panax quinquefolius saponin; PJSM: The total saponins of Panax japonicus; PJPS:
The crude polysaccharides of Panax japonicus; G-Rh2-B2: derivative B2 of ginsenoside Rh2; PPQN: neutral polysaccharide from Panax quinquefolius; PNFS: Panax
notoginseng flower saponins; SLPF: stem and leaf of Panax notoginseng flavonoid; GOP: Ginseng oligopeptides; WGP: water-soluble ginseng polysaccharide; TSPJ: Total
Saponins of Panax japonicus; RG-CW-EZ-CP; TGCG: total ginsenosides in Chinese ginseng; RGEF: hydrophobic fraction of red ginseng ethanol extract; WGPA: acidic
polysaccharide of ginseng; Pg-C-EE: ethanolic extract of P. ginseng berry calyx; AF: Arginyl-fructose; AFG: arginyl-fructosyl-glucose; PA: Pyroglutamic acid; GTS:
ginseng total saponin); LPNS: Leaves of Panax notoginseng saponin.
6.4. Neuroprotective activity
With the increase of population aging and social life pressure,

people are more and more exposed to the risk of nervous system dis
eases. Common neurological disorders include Alzheimer's disease
(AD), Parkinson's disease, epilepsy and depression. Ginsenosides play
an increasingly important role in the treatment of nervous system dis
eases, especially in the central nervous system. Several mechanisms
were identified to exhibit significantly neuroprotective activity in
cluding the elimination of free radicals to activate brain function, in
hibition of oxidative stress and neuroinflammation, the lower levels of
toxins-induced apoptosis and regulation of N-methyl-Daspartate re
ceptor channel activity (González-Burgos et al., 2015). Fig. 4 showed
the multiple possible neuroprotective mechanisms for extracts and
ginsenosides from Panax. The abnormal increase of Ca2+ level was an
important indicator of neurological disorders, which could increase the
risk of epilepsy. Take ginsenosides as an example, total ginsenosides
and ginsenoside Rg3 (18) could restrain the increase of Ca2+ induced
by Mg2+ (Kim and Rhim, 2004). Besides, studies showed that ginse
noside Rb2 (14) had the potential to become an anticonvulsant drug
(Lian et al., 2006). Pseudoginsenoside F11 (225) could also be a valu
able option to slow down the process of neurodegenerative disease.
Zhang et al. discovered that pseudoginsenoside F11 (225) had beneficial
effects on the pathological changes of AD in senescence accelerated
mouse P8 (SAMP8). The possible mechanisms for improving cognitive
impairment act were inhibition of beta-site amyloid precursor protein
cleaving enzyme 1 (BACE1) activity and enhancement of protein
Fig. 3. The structure of some compounds with antineoplastic activity.
phosphatase 2A (PP2A) activity (Zhang et al., 2019a,b).
played an immune regulatory role through many ways, such as immune

6.5. Immunoregulatory activity
organs (thymus, spleen), immune cells (macrophages, dendritic cells,
natural killer cells, etc.) and cytokines (TNF-α, IFN-γ, IL-2, IL-6, IL-12,
Modern pharmacological studies showed that ginseng was the
etc.) (Bai et al., 2019). Ginsenosides and ginseng polysaccharide were
adaptogenic drug, which had bidirectional regulation to be conducive
the main active components of P. ginseng with a wide range of appli
to the recovery and enhancement of body functions (Dou et al., 1999).
cations in immune regulation (Wang and Wang, 2005). P. ginseng pectin
Ginseng could also be considered as an immunomodulator, which
Fig. 2. The comparison of different biological activity related to chemical components reported from the genus Panax.
32
SB was isolated from P. ginseng root to have a bidirectional regulation 6.8. Hemostasis and activating blood stasis activity of P. notoginseng
effect on human monocyte THP-1, secreting cytokine interleukin-8 (IL-
8) and IL-2 by mouse spleen cell (Tian et al., 2011a,b). Low con The root of P. notoginseng, characterized by the presence of Rb1 (13),
centrations of ginseng pectin promoted the secretion of immune cyto Rd (17) and Rg1 (97) levels, was described as a unique herb for in
kines, while high concentrations of ginseng pectin inhibited the process. vigorating the circulation of blood and hemostasis. Dencichine was a
Similar immunologically active chemical components have also special amino acid isolated from the roots of P. notoginseng. It could
been found in other species of the Panax. In addition, Zhu et al. isolated shorten the bleeding time of mice and reduce activated partial throm
and purified a galactoside (PPQ) from the roots of P. quinquefolius (Zhu boplastin time (APTT) and thrombin time (TT), while the concentration
et al., 2012). The results showed that PPQ might be expected as a po of fibrinogen (FIB) in plasma would increase in a dose-dependent
tential antitumor drug with immunoregulatory activity. At a high dose manner. Meanwhile, studies showed that dencichine exerted hemos
of 400 mg/kg, the production of IL-2 and IFN-γ was significantly in tasis activity by regulating intracellular cAMP levels (Huang et al.,
creased and the expression of IL-10 was decreased. Then, it regulated 2014). Owing to the stability of dencichine was easily destroyed at high
the secretion of Th1/Th2 cytokines to enhance immunity. P. notoginseng temperature, P. notoginseng should be used for hemostasis without
saponins (PNS) possessed immnologic adjuvant activities and enhanced heating. In addition, the active substances for hemostasis contained
the humoral and cellular immune responses to ovalbumin (OVA) in calcium ions and quercetin (Dong et al., 2003). Other studies found that
mice when administered with OVA (Sun et al., 2003). PNS had great impact on blood-activating through anticoagulation and
antiplatelet aggregation. It suggested that P. notoginseng had a dual-
directional regulation of hemostasis and blood-activating (Liu et al.,
6.6. Cardioprotective activity
2018a,b,c,d). Some studies also confirmed the dose-effect relationship
of P. notoginseng. It was found that the small-dose application mainly
As cardiovascular disease is becoming the major cause of mortality
showed the effect of hematuria, while with the increase of the dose of
and the limitations of conventional drugs used in therapy, the devel
P. notoginseng, its blood-activating effect was enhanced (Yu et al.,
opment of new active substances from medicinal plants is needed in the
2008). Otherwise, the study also confirmed the hematopoietic function
current clinical and experimental research (Adegbola et al., 2017).
of P. notoginseng. The main mechanism was that PNS could induce the
Phenolic acids, saponins, flavonoids, alkaloids and other compounds in
synthesis of GATA 1 and GATA 2 transcriptional regulatory proteins in
Panax have better pharmacological activities against myocardial
hematopoietic cells, thereby regulating the expression of genes related
ischemia. The research on cardiovascular diseases mainly focuses on
to hematopoietic cell proliferation and differentiation (Gao et al.,
the purified ginsenoside monomers from P. ginseng rather than the
2004).
whole extracts. The most frequently studied ginsenosides are Rg1 (97),
Rb1 (13), Rh1 (100), Re (104) and Rd (17) (Kim, 2012). The extracts of
6.9. Other biological activities
P. ginseng can promote collateral circulation to alleviate myocardial
ischemia symptoms. Ginseng stem leaf glucoside can resist chloroform-
In modern research, it was reported that the Panax had various
induced arrhythmias in mice and prevent aconitine-induced ar
other biological activities in addition to those listed above. A series of
rhythmias in mice (Tang et al., 2009). Ginsenoside Re (104) has a
evidence also indicated that ginsenosides could alleviate the pain
therapeutic effect on triggering ventricular arrhythmia. However, it can
caused by toxic chemicals in experimental animals. For example, gin
cause poisoning or side effects due to the strong tonic effect, if P. ginseng
senoside Rf (102) inhibited voltage-dependent Ca2+ channels and al
is misused or overused (Yang, 2009).
leviated the pain reactions induced by a chemical stimulus (Mogil et al.,
P. notoginseng is also an effective anti-angina medicine. It was
1998). Ginsenoside Rd (17) inhibited the transmission of pain by reg
quantitatively confirmed in Lei's study that water extracts of
ulating the central signaling molecule PKCγ (Gao et al., 2017). The
P. notoginseng improved the cardiovascular function in a dose-related
analgesic mechanisms of ginseng glycopeptides (GGT) might be related
manner (Lei et al., 2012). The research showed that P. notoginseng in
to the regulation of pro-inflammatory cytokines (IL-1, TNF-α) and the
creased coronary blood flow and cardiac contractility without changing
dynamic balance of anti-inflammatory cytokines (IL-2, IL-4) (Tian et al.,
heart rate. In addition, Xu et al. showed that P. quinquefolius 20(S)-
2018). The central analgesic activity of ginsenosides metabolite com
protopanaxadiol saponins (PQDS) had cardioprotective effects in vivo
pound K (CK, 74) was evaluated by the hot plate method. The results
and in vitro (Xu et al., 2013). The mechanism might eliminate the lipid
showed that CK could reduce the number of writhing caused by acetic
peroxidation products and enhance the function of the endogenous
acid and increase the pain threshold of carrageenan-induced in
antioxidant enzymes.
flammatory pain, suggesting that 74 has peripheral analgesic effects (Si,
2018).
6.7. Antidiabetic activity In addition, the aboveground parts of P. notoginseng had the effect of
restraining the central nervous system, which were characterized by
Since the existing synthetic drugs are often accompanied by con sedation, stability and improvement of sleep. PNS and ginsenoside Rb1
siderable side effects, natural hypoglycemic compounds may be effec (13) had the coordination effects of with central depressant drugs.
tive and safe alternatives to the treatment of diabetes or currently used Although there was relatively limited researches about the toxicity of
therapeutic enhancers (Coman et al., 2012). According to the research P. notoginseng, several phenomena had been proved that R1 (119), Rg1,
of Chen et al., P. notoginseng was one of the promising medicinal plants Re, Rb1, Rg2 and Rd could inhibit the germination of P. notoginseng
had great ability of antidiabetes and antiobesity. PNS and dammarane seeds and had obvious autotoxicity to root cells (Yang et al., 2015). The
saponins were the main bioactive components in P. notoginseng (Chen possible mechanism was that saponins inhibited the synthesis of in
et al., 2008). At present, the hypoglycemic and anti-obesity character tracellular antioxidants in the roots of P. notoginseng, leading to the
istics of PNS are widely reported. PNS had the antidiabetic and anti excessive accumulation of oxygen free radicals. (Xu et al., 2015).
obesity effects on KK-Ay mice with type 2 diabetes and its preventive
effects on renal lesions (Uzayisenga et al., 2014; Tang et al., 2016). 7. The application and development of Panax classical
According to literature review, the main mechanisms of PNS exerting prescriptions in modern pharmacology
anti-diabetic activity were: (1) reducing glucose uptake, lipogenesis; (2)
increasing glucose absorption; (3) reducing gluconeogenesis and in With validated safety and reliability, many classical prescriptions in
hibiting glycogenolysis; (4) increasing insulin sensitivity and reducing TCMs have been used for thousands of years. This record of long-term
insulin resistance. clinical experience can provide a more reliable therapeutic basis than
33
Fig. 4. Several neuroprotection mechanisms of ginsenosides.
the laboratory research with relatively limited time based on modern have shown remarkable medicinal value such as in adjuvant therapy for
pharmaceutical standards. Moreover, studies suggested that many tumor and resuscitation of hemorrhagic shock. In addition, their related
classical prescriptions were of good research value. For instance, bo compounds have been developed into new drugs. Hence, in the present
jungikki-tang (bu zhong yi qi tang in Chinese) was a prescription study, we have comprehensively reviewed the components and bioac
composed of eight TCMs including Ginseng Radix and Astragali Radix, tivities of the known metabolites from Panax and critically discussed
which had been extensively used in China, Korea and Japan owing to the applications and issues of limited availability. To date, at least 748
the therapeutic efficacy on the weakness of spleen and stomach. chemical compounds from genus Panax have been isolated, such as
Modern pharmacological studies showed that bojungikki-tang had an saponins, flavonoids, polysaccharide, steroid and phenols. Saponins are
tibacterial activity and exhibited positive outcomes in murine models of considered as the major bioactive components, among which PPD (Rg3,
chronic fatigue syndrome (CFS) (Yan et al., 2002). Moreover, clinical Rb1, Rb2, Rc and Rd) and PPT type ginsenosides (Rg1, Re and Rg5) are
studies confirmed the beneficial effects of bojungikki-tang on cancer- the most widely distributed in Panax plants. These ginsenosides can be
related fatigue (Jeong et al., 2010). Saengmaee-san (Sheng mai san in recommended as the characteristic indicators for quality evaluation and
Chinese) was composed of three herbs (Ginseng Radix, Schisandrae identification. However, studies on flavonoids, polysaccharides and
Fructus and Ophiopogon Rhizome). It had been proved to exhibit an acetylenic alcohols are inadequate compared to those on saponin
tioxidant effect in vitro and in vivo and could treat heart failure and components. Moreover, limited attention has been paid to some species
other cardiovascular diseases (Ichikawa and Konishi, 2002). In view of such as P. sokpayensis, P. stipuleanatus, etc. It is feasible to use bioac
the synergetic and regulatory effects among various components, tivity-oriented separation strategies to identify more bioactive compo
compound preparations may become a novel therapeutic choice to nents. Further phytochemical studies are suggested to focus on the
maintain the balance of Yin and Yang in human body in the future. species with less research or better efficacy chemical components.
Therefore, the modern investigation of the TCMs preparations in the Additionally, further study concerning single chemical component of
ancient classical prescription may also be another potential method for Panax is inseparable from the diverse chemical structure, significant
drug development. biological activity and clinical application. The discovery of the
bioactive molecules and multicomponent interactions could provide
great significance to the clinical application of Panax plants. For in
8. Conclusion and future perspectives stance, the binding of ginsenoside Rg1 to ginsenoside Rb1 triggers the
loss suppression of oxidative stress and inflammatory factors via
Genus Panax, globally-recognized tonic Chinese herbal medicines,
34
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LL, F-RX, and Y-ZW conceived the review. LL and F-RX collected trials to determine the pharmacokinetics, safety, tolerability, and sex effect of oral
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Chen, J., Liu, G., Sun, Q., Zhang, F., Liu, C., et al., 2019. Protective effects of ginsenoside
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Declaration of competing interest naling pathway. Life Sci. 216, 1–9. https://doi.org/10.1016/j.lfs.2018.11.022.
Cho, J.Y., Yoo, E.S., Baik, K.U., Park, M.H., Han, B.H., 2001. In vitro inhibitory effect of
protopanaxadiol ginsenosides on tumor necrosis factor (tnf)-α production and its
The authors declare that there is no conflict of interest regarding modulation by known tnf-α antagonists. Planta Med. 67, 213–218. https://doi.org/
publication of this Paper. 10.1055/s-2001-12005.
Cho, W.C.S., Chung, W., Lee, S.K.W., Leung, A.W.N., Cheng, C.H.K., et al., 2006.
Ginsenoside re of Panax ginseng possesses significant antioxidant and antihyperlipi
Acknowledgments demic efficacies in streptozotocin-induced diabetic rats. Eur. J. Pharmacol. 550,
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This work was supposed by National Natural Science Foundation of Cho, Y., Son, H., Kim, K., 2014. A 14-week randomized, placebo-controlled, double-blind
clinical trial to evaluate the efficacy and safety of ginseng polysaccharide (Y-75).
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Atividades Biolgicas de Compostos Vegetais

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Journal of Ethnopharmacology 263 (2020) 112792

Contents lists available at ScienceDirect

Traditional uses, chemical diversity and biological activities of Panax L. T

ARTICLE INFO ABSTRACT:

Panax assamicus R.N.Banerjee Species – Assam and East Himalaya

Note. ∗Cited from the website: https://www.wiki8.com/.

PPD type saponins core structure

NO. Compound R1 R2 R3 R4 C20

NO. Compound R1 R2 R3 R4 C20

PPT type saponins core structure

95 20(S)- protopanaxatriol H H H OH CH3

118 20(R)-ginsenoside Rh19 Glc H H CH3 OH

178 Malonyl-floralginsenosides Re1 H (6-Mal)Glc2-Rha H O-Glc CH3

OA type saponins core structure

188 Taibaienoside IV Glc-UA2-Glc CH3 H

198 Bifinoside A Ara(p) H H COOCH3 CH3 H

OC type saponins core structure

NO. Compound R1 R2 R3 C20 C24

221 Gypenoside F11 H O-Glc-Rha CH3 R S

240 24(S)-6-O-[β-D-glucopyranosyl-(1 → 2)-β-D-glucopyranosyl]-dammar-20,25-epoxy-3β,6α,12β,24α-tetraol H Glc2-Glc CH3 S S

Note: Glc: β-D-glucopyranosyl; Xyl: β-D-xylopyranosyl; Rha: α-L-rhamnopyranosyl; AC: acetyl.

PPD C17-side chain varied

246 V1 25-hydroxy-23-ene-20(S)-protopanaxadiol H OH OH – C24:S

NO. Type Compound R1 R2 R3 R4 Chiral Carbon

PPT C17-side chain varied

(continued on next page)

NO. Type R1 R2 R3 R4 R5 R6 Chiral Carbon

(continued on next page)

365 W8 O-Glc2-Glc OH H Glc6-Glc OH – C24:R

366 W8 OH O-Glc H H OH – C24:R

(continued on next page)

420 W27 O-Glc H H OH – – –

NO. Type Compound R1 R2 R3 R4

465 A Baisanqisaponin A H H X Glc

(continued on next page)

Then, a flavonoid glycoside, quercetin-3-O-sophora glycoside was ob­

quefolius (Zhang et al., 2002a,b).

5.4. Polyacetylenes (546–568)

Alkyne hydrocarbons are less distributed in Panax, mainly in the

0.033% respectively, which had strong inhibitory effects on staphylo­

(0.077%) (Duan et al., 2008). Zhou et al. analyzed the polyacetylene

components was higher in the main roots, flowers and rhizomes of

(546) in P. notoginseng flower was higher, but panaxydol (548) could

hardly be detected. In addition, wei et al. isolated seven polyacetylenes

from the underground part of P. vietnamensis, two of which were newly

(547), ginsenoynes B (549), ginsenoynes C (552), ginsenoynes D (553)

root of P. ginseng (Hirakura et al., 1991), whose structures were de­

5.5. Polysaccharides (569–598)

Biologically important polysaccharides have been less widespread

from the rhizomes of P. japonicus plants, the roots of P. quinquefolius,

P. notoginseng plants and the flower buds of P. ginseng.

5.6. Fatty acids (599–621)

Lipid is an important component of P. ginseng. Fatty acid compounds

Biological Activities Name Description In vivo/In Reference

Biological Activities Name Description In vivo/In Reference

Biological Activities Name Description In vivo/In Reference

Biological Activities Name Description In vivo/In Reference

PNS raised levels of 5-hydroxytryptamine (5-HT), DA and In vitro Wu (2003)

Biological Activities Name Description In vivo/In Reference

Then, a flavonoid glycoside, quercetin-3-O-sophora glycoside was ob

0.033% respectively, which had strong inhibitory effects on staphylo

root of P. ginseng (Hirakura et al., 1991), whose structures were de