Department of Biochemistry, Major S D Singh Medical College & Hospital, Fatehgarh (U.P.), India Tel: 7607879471
Department of Biochemistry, Major S D Singh Medical College & Hospital, Fatehgarh (U.P.), India Tel: 7607879471
Department of Biochemistry, Major S D Singh Medical College & Hospital, Fatehgarh (U.P.), India Tel: 7607879471
Department of Biochemistry, Major S D Singh Medical College & Hospital, Fatehgarh (U.P.), India
Email: [email protected]
Tel: 7607879471
Subodh Kumar
Department of Biochemistry,
Major S
D Singh Medical College &
Hospital,
Fatehgarh (U.P.), India
Kiran Saxena
Department of Biochemistry,
Chirayu
Medical College & Hospital,
Bhopal
(M.P.) India
Uday N. Singh
Department of Biochemistry,
Major S
D Singh Medical College &
Hospital,
Fatehgarh (U.P.), India
Ravi Saxena
Department of Biochemistry,
Chirayu
Medical College & Hospital,
Bhopal
(M.P.) India
Correspondence:
Subodh Kumar
components, property, Chemical composition, Mechanism of action, function, side effects, current
research and their potential application in modern medicine. The present study demonstrates that ginger
showed broad spectrum action in which Anti-inflammatory action is one of them. So the present study
concludes that ginger and its bioactive components have the potential for development of modern
medicine in the treatment of anemia and various diseases in near future.
1. Introduction
Anemia of inflammation is considered a major contributor to anemia observed in developing
countries [ 1] and anemia of inflammation may even be associated with asymptomatic and
Anti- subclinical infection [2]. The only effective treatment of chronic inflammation is correction of
inflammatory the underlying disorder [3]. NF-κB is a pleiotropic transcription factor. It is involved in the
transcriptional activation of numerous genes leading to a cumulative immunogenic response,
action of provides a molecular link between the innate and adaptive immune system, whilst playing
regulatory roles in haemapoiesis and lymphoid organogenesis. NF-κB activation seems to be a
key early event in a variety of cell & animal model systems developed to elucidate the
ginger: A pathobiology of lung disease including Systemic inflammatory [4].
Ginger is extensively used as a spice & food preservative in India, China and South East Asia
critical and probably originated in India. [5, 58] Ginger obtained from the underground stems of
rhizomes of Zingiber officinale Rosc.), an herbaceous tropical perennial belonging to the
review in family Zingiberaceae. It has been used in Ayurvedic Medicine since ancient times with various
biological applications. Different constituents of ginger has been established its role in
anemia of medicine to treat various ailments from time immemorial in different parts of the world [6].
Recent years have seen an increased enthusiasm in treating various diseases with natural
inflammation products. Ginger (Zingiber officinale) is a non- toxic highly promising natural antioxidant
compound having a wide spectrum of biological function (antimicrobial, anti- inflammatory,
and its future antioxidant, immunomodulatory, anticarcinogenic). Safety evaluation studies indicate that
Zingiber officinale are well tolerated even at a very high dose without any toxic effects [7].
aspects Thus ginger and its bioactive components have the potential for development of modern
medicine in the treatment of anemia and inflammation associated diseases
ABSTRACT
Anti-inflammatory action of
ginger has been confirmed
by various scientists, but
there is very few review
article published till date on
inflammation associated
diseases. Inflammation is
mainly, culprit of anemia
and inflammation
associated disorder (like-
Pulmonary diseases,
Cardiovascular diseases,
Diabetes Type-2, cancer,
Arthritis, Alzheimer,
Neurological diseases and
Autoimmune
diseases).Since Infection
(bacterial/ viral), activate
Nuclear factor –-κB, which
is a major mediator of
inflammation in most of the
disease. Zinger has been
established potent NF–ƙB
inhibitory action via the
suppression of pro-
inflammatory cytokine,
TNF-α and also provides a
molecular link between the
innate and adaptive immune
system. This review takes
the Zinger bioactive
International Journal of Herbal Medicine
(like- Pulmonary diseases, cardiovascular diseases, Diabetes Type- the gingerol series (Table 1). The powdered rhizome contains 3-6%
2, cancer, Arthritis, Alzheimer, Neurological diseases and fatty oil, 9% protein, 60-70% carbohydrates, 3-8% crude fiber,
autoimmune diseases) in near future cost effectively, the main aim about 8% ash, 9-12% water and 2-3% volatile oil. The volatile oil
of the present review. consists of mainly mono and sesquiter–penes; camphene, beta-
phellandrene, curcumene, cineole, geranyl acetate, terphineol,
2. Review of Literature terpenes, borneol, geraniol, limonene, linalool, alpha-zingiberene
2.1 Chemistry of zinger (30-70%), beta-sesquiphellandrene (15-20%), beta-bisabolene (10-
In the fresh ginger rhizome, the gingerols were identified as the major 15%) and alpha-farmesene. In dried ginger powder, shogaol a
active components and [6] gingerol [5-hydroxy-1-(4-hydroxy-3- dehydrated product of gingerol, is a predominant pungent
methoxy phenyl) decan-3-one is the most abundant constituent in constituent upto [8-10].
Table 1: Structure of active component of ginger with IUPAC name
1. 6-gingerol (S)-5-hydroxy-1-(4-hydroxy-3-methoxyphenyl)-3-decanone
2. 8- gingerol (5S)-5-hydroxy-1-(4-hydroxy-3-methoxyphenyl) dodecan-3-one
3. 10-gingerol (E)-1-(4-hydroxy-3-methoxyphenyl) dec-4-en-3-one
4. 6-shogaol (E)-1-(4-Hydroxy-3- methoxyphenyl) dec-4-en-3-one
2.2 Chemical Composition of ginger: Nutritional data for 100 observed that two labdanum-diterpene like dialdehides isolated
gm. Dry ginger is as follows from Ginger extracts act as in vitro inhibitors of the human 5-
Water–9.4 gm, Protein–9.1gm, Fat–6.0gm, Total carbohydrate– lipooxygenase [35]. In one study curcumin has been shown to
70.8 gm, Food energy–374 kcal, Fibre–5.9 gm, ash–4.8 gm, iron– suppress the expression of COX2, 5-LOX, and iNOS, most likely
12 mg, magnesium–184 mg, Phosphorous- 148 mg, potassium- through the downregulation of NF-κB activation [ 36]. The other
1342 mg, sodium-32 mg, zinc–5 mg and niacin-5mg [11]. study reported that 6-gingerol, a natural analog of curcumin
derived from the root of ginger (Zingiber officinalis ), exhibits a
2.3 The percentage of vitamin in ginger rhizome powder is as
biologic activity profile similar to that of curcumin [37].
follows
Thiamine–0.035%, Riboflavin–0.015%, Niacin–0.045%, 2.7 Anti-inflammatory action of ginger
Pyridoxin–0.056%, Vitamin C–44%, vitamin A-Traces, vitamin E- The anti-inflammatory properties of ginger have been known and
valued for centuries. The original discovery of ginger's inhibitory
Traces, Total-44.15% [12]. effects on prostaglandin biosynthesis in the early 1970s has been
2.4 Ginger: safety, dose, side effect and drug interactions repeatedly confirmed. This discovery identified ginger as an herbal
Safety: Ginger is recommended in U.S. Food and Drug medicinal product that shares pharmacological properties with non-
Administration’s GRAS (generally recognized as safe) list.The steroidal anti-inflammatory drugs. Ginger suppresses prostaglandin
British Herbal Compendium documents no adverse effects of synthesis through inhibition of cyclooxygenase-1 and
ginger [13]. Ginger appears to be relatively safe except in pregnancy cyclooxygenase-2. An important extension of this early work was
[14]. the observation that ginger also suppresses leukotriene biosynthesis
Dose: A dose of 0.5–1.0 g of ginger powder ingested 2-3 times for by inhibiting 5-lipoxygenase. This pharmacological property
periods ranging from 3 months to 2.5 years did not cause any distinguishes ginger from nonsteroidal anti-inflammatory drugs.
adverse effects [ 15]. Most of the research has been done with 1-2 This discovery preceded the observation that dual inhibitors of
grams of ginger powder, but in India the average intake is around cyclooxygenase and 5-lipoxygenase may have a better therapeutic
8-10 grams per day. profile and have fewer side effects than non-steroidal anti-
inflammatory drugs. The characterization of the pharmacological
Side effect: Ginger is quite safe in therapeutic doses. For anti- properties of ginger entered a new phase with the discovery that a
inflammatory purpose, the dose of ginger is 3–6 grams two to three ginger extract (EV.EXT.77) derived from Zingiberofficinale (family
times per day. In experimental animals, the doses of 2.5 gram/kg Zingiberaceae) and Alpinagalanga (family Zingiberaceae) inhibits
the induction of several genes involved in the inflammatory
body weight were tolerated without any mortality. However, when
response. These include genes encoding cytokines, chemokines,
the dose was increased to 3–3.5 gram/kg body weight then there
and the inducible enzyme cyclooxygenase-2. This discovery
was 10–30 % mortality [16]. provided the first evidence that ginger modulates biochemical
Drug interaction: Few ginger–drug interactions have been pathways activated in chronic inflammation. The earlier report
suggested that in Rheumatoid arthritis (RA) and Osteoarthritis
reported in the literature. Ginger does not interact with the anti-
(OA) patients, use of powdered ginger for 3-month to 2.5-year
coagulant drug warfarin in rats or man [17- 18]. period, reduce pain and inflammation in 75% patients without any
2.5 Functional property of Ginger: Ginger, as an antimicrobial adverse effect and suggested ginger is an anti-inflammatory agent [
[19-21] 24]
, anti-inflammatory [22-29], antioxidant [30--32] and . 6-gingerol acts as an anti-inflammatory compound that may be
useful to treat inflammation without interfering with antigen
immunomodulatory role [26] have been established.
presenting function of macrophages [38]. It has been also recently
2.6 Mechanism of action of ginger observed that Synergistic effect of Ginger with anti- tuberculosis
Ginger is considered to exert its anti-inflammatory activity by treatment were more beneficial effect rather than only ATT (anti-
inhibiting COX-2 and LOX pathways [33-34]. Recently, it has been tuberculosis treatment) in anemic Pulmonary
~ 17 ~
International Journal of Herbal Medicine
tuberculosis Patients and concluded that ginger supplementation in serum iron, total iron binding capacity, which in turn correct
such patients not only increases absorption of iron but also
anemia [29].
significant decreases in CRP, Ferritin and significant increase in
Fig 1: Synergetic effect of anti- tubercular treatment (ATT) with ginger supplementation a new approach to cure TB with better outcome.
2.8 Antimicrobial Action (8-gengerol and 10 gingerol) were more active, with MIC values of
Investigation of ginger rhizome (Zingiber officinale) afforded three
25–50 μg/ ml exhibited towards M. tuberculosis H37Rv and M.
lipophilic analogues 6-gingerol [39]
, 8-gingerol [40]
and 10- gingerol [ avium [40, 41].
41]
that exhibited antimicrobial activity. The lipophilic analogues
2.9 Pathophysiological Mechanism underlying Anemia of found to mediate a wide variety of diseases including cardiovascular
inflammation diseases, diabetes, arthritis, Alzheimer’s disease, pulmonary diseases
Anemia of inflammation Pathophysiology is like Anemia of and autoimmune diseases. Chronic inflammation has also been
Chronic disease (ACD) [60]. During inflammation, hepcidin (an associated with various steps involved in carcinogenesis as well as
acute phase protein) production is stimulated and iron entry into cellular transformation, promotion, survival, proliferation, invasion,
plasma is inhibited, causing the hypoferremia and anemia of angiogenesis and metastasis [46-47]. Many pro-inflammatory cytokines
inflammation [42]. Acute Phase Proteins are a class of diverse can activate the transcriptional factor NF-κB, while some of the effects
Proteins whose blood plasma concentrations increase (positive of pro-inflammatory cytokines may be mediated through the NF-κB
acute phase protein), or decreases (negative acute phase protein) pathway [48-50].
during the response to inflammation in the acute phase. They are
produced within a few hours by the liver, responding to 2.11 Role of Bioactive component of Zinger
inflammatory cytokines such as IL-1, TNF-α and in particular IL-6 The 6-gingerol and 6-paradol have been reported to possess a
[43-44, 59]
. It has been observed that during infection, there is an strong anti-inflammatory activity and to suppress the TNF-α
increase in cytokine levels (IL-6) which is responsible for production in TPA-treated female ICR-mice and rats [51, 52]. The
activation of NF-κB & endotoxins which in turn increase the activation of the TNF-α gene causes the release of pro-
synthesis and release of CRP from hepatocytes. Raised level of inflammatory cytokines, and this would activate the transcriptional
CRP is marker of inflammation which causes blunted factor NF-κB. Activation of NF-κB would activate the expression
erythropoietin resistance resulting anemia. of other inflammatory cytokines such as COX-2, LOX-2, other
chemokines and iNOS, which would lead to inflammation and
2.10 Various disorders linked with anemia of inflammation related diseases. Ginger (Zingiber officinale) is widely used all
Inflammation is considered to play an important role in the over the world as a spice and condiment in daily cooking. It is a
Pathophysiology of various disorders. However, when natural food component with many active phenolic compounds
inflammation becomes chronic or lasts too long, it can be harmful. such as shagaol and gingerol, and it has been shown to have broad
The diagnosis of inflammation and its biomarkers are not fully anti-inflammatory action. It is apparent that ginger may act as an
understood; however, pro-inflammatory cytokines, chemokines, anti-cancer and anti-inflammatory agent by blocking the activation
adhesion molecules and the inflammatory enzymes have been of NF-κB via the suppression of pro-inflammatory cytokine, TNF-
[53]
linked to chronic inflammation [45]. Chronic inflammation has been α . Other, similar reports have also shown the inhibitory effect of
~ 18 ~
International Journal of Herbal Medicine
ginger on the NF-κB pathway: topical application of 6-gingerol chronic treatments & finally concluded that although there are
inhibited TPA-induced COX-2 expression and suppressed NF-κB some problems limiting the development of phytomedicine, such as
DNA binding activity in mice skin [51, 54]. The 6-gingerol and 6- lack of standardization, efficacy and quality control of plants used,
paradol have been reported to possess a strong anti-inflammatory extinction of some plant species, lack of funds and others, if these
activity and to suppress the TNF-α production in TPA-treated problems can be fully addressed, this will help in the future
female ICR-mice and rats [51, 52]. Inhibiting the activity of NF-κB, development and harmonization of phytomedicines [57]
will subsequently inhibit inflammation and inflammation
associated disorder. The natural active compounds in ginger 3. Discussion & Conclusion
(gingerols and zerumbone) have been found to be potent inhibitors On the basis of above mention review of literature we found that
for NF-κB and pro-inflammatory cytokine TNF-a. Ginger may inflammation and acute phase response interact with iron
block any one or more steps in the NF-κB signaling pathway, such metabolism, which leads to disregulation of iron metabolism
as the signals that activate the NF-κB signaling cascade, resulting anemia. NF-κB activation is a major mediator of
translocation of NF-κB into the nucleus, DNA binding of dimers or inflammation in most of the disease (like- Pulmonary diseases,
interactions with the basal transcriptional machinery [55]. Cardiovascular diseases, Diabetes Type-2, cancer, Arthritis,
Ginger extract significantly reduced the elevated expression of NF- Alzheimer, Neurological diseases and Autoimmune diseases), and
κB and TNF-α in rats with liver cancer. Ginger may act as an anti- inhibition of NF-κB activation can suppress inflammation.Over
cancer and anti-inflammatory agent by inactivating NF-κB through expression of NF-κB, COX2, 5-LOX, and iNOS leads to
the suppression of the pro-inflammatory TNF-α [56]. inflammation and inflammation associated disorder. Since Ginger
has potent NF-κB inhibitory action, it suppresses the expression of
2.12 Zinger future perspective COX2, 5-LOX, and iNOS, most likely through the downregulation
As a source of potential chemotherapeutic agent continues. Natural of NF-κB activation.Ginger may act as an anti -inflammatory agent
products and their derivatives represent more than 50% of all the by blocking the activation of NF-κB via the suppression of pro-
drugs in clinical use in the world today. Phytomedicine have more inflammatory cytokine, TNF-α. (Fig. 3)
beneficial effect than their synthetic counterparts through being
safer, acceptable, affordable, culturally compatible and suitable for
Fig 3: Ginger Supplement inhibits both COX- 2 & LPO expression by suppressing NF- ƙB activity via TNF – α
This review article concludes that ginger and its bioactive Free Press Ltd. Brattleboro Vermont USA 1994; 111-125.
components have the potential for development of modern 7. Brinker F. Herb contraindications and drug interactions. Edn 2.
medicine in the treatment of various diseases in near future because Sandy, OR: Eclectic Medical; 1998.
it controls the molecular mechanism of inflammation. Further trials 8. Mustafa T, Srivastava KC, Jensen KB. Drug Development Report
(9): Pharmacology of ginger, Zingiber officinale. J Drug Dev 1993;
in humans are required to determine the efficacy of ginger (one or
6(24).
more of its constituents) and to study what, if any, beneficial or 9. Kiuchi F, Shibuya M, Sankawa V. Inhibitors of prostaglandin
adverse effects are observed if consume over a long period of time. biosynthesis from ginger. Chem Pharm Bull 1993; 30:754.
10. Awang DVC. Ginger, CPJRPC July1992; 309.
4. Reference 11. Farrel KT. Spices, Condiments and Seasonings.The AVI Publ.Co. Inc;
1. Abshire TC. The anaemia of inflammation: a common cause of Westport, CN, USA, 1985.
childhood anaemia. Pediatr Clinics North America 1996; 43:623–638. 12. Haq F, Faruque SM, Islam S, Ali E. Studies on Zingiber officinale
2. Vanden BNR, Letsky EA. Etiology of anaemia in pregnancy in south Roscoe. Part 1. Chemical investigation of the rhizome. Bangladesh. J
Malawi. Am J Clin Nutr 2000; 72:47–56. Sci Ind Res 1986; 21(1-4):61-69.
3. Andrew NC, Erdjument BH, Davidson MB, Tempst P, Orkin SH. 13. Bradely P, ed. British Herbal Compendium. Bournemouth:British
Erythroid transcription factor NF-E2 is a haematopoietic specific Herbal Medical Association, 1990.
basic leucine Zipper protein. Nature 1993; 362: 722-728 14. Alternative Therapies. Am J Health–Sys Pharm May 15, 2000; l57.
4. John WC, Ruxana TS, Timothy SB. CHEST 2000; 117:1482-1487. 15. Langner E, Greifenberg S, Gruenwald J. Ginger: History and use.
5. Purseglove JW, Brown EG, Green CL, Robbins, SRJ. Longman Inc, Adv Ther 1998; 15:25.
New York 1981; 2. 16. Srivastava KC. Aqueous extracts of onion, garlic and ginger inhibit
6. Schulick P. Ginger-common spice and wonder drug. Edn 2. Herbal
~ 19 ~
International Journal of Herbal Medicine
platelet aggregation and alter arachidonic acid metabolism. Biomed 39. Igarashi M, Hayashi C, Homma Y, Hattori S, Kinoshita N, Hamada
BiochimActa 1984; 43(8-9):S335-346. M, Takeuchi T, J Antibiot 2000; 53:1096.
17. Weidner MS, Sigwart K. The safety of a ginger extract in the rat. J 40. Takeuchi T, Igarashi M, Naganawa H, Hamada M. 2001, JP
Ethnopharmacol 2000; 73: 513–520. 2001055386.
18. Vaes LP, Chyka PA. Interactions of warfarin with garlic, ginger, 41. Kondo S, Yasui K, Katayama M, Marumo S, Kondo T, Hattori H,
ginkgo, or ginseng: nature of the evidence. Ann Pharmacother 2000; Tetrahedron Lett 1987; 28:5861.
34: 1478–1482. 42. Tomas G. Molecular control of Iron Transport. J Am Soc Nephrol
19. Yamada Y, Kikuzaki H, Nakatani N. Identification of Antimicrobial 2007; 18:394-400.
Gingerols from Ginger (Zingiber officinale Roscoe), J Antibact 43. TRE JE et al. The acute phase response and the haematopoietic system:
Antifung Agents 1992; 20(6):309–11. The role of cytokines. Crit Rev Oncol Hemato 1995; 21:1-18.
20. GalaL AM. Antimicrobial Activity of 6-paradol and Related 44. Epstein FH: Acute Phase Proteins and other systemic responses to
Compounds, Int. J Pharmacogn 1996; 34(1):64–9. inflammation. N Engl J Med 1999; 340:448-454.
21. Hiserodt RD, Franzblau SG, Rosen RT. Isolation of 6-, 8-, 10- 45. Ohshima H, Tatemicho M, Sawa T. Chemical basis of inflammation-
Gingerol from Ginger Rhizome by HPLC and Preliminary Evaluation induced carcinogenesis. Arch. BiochemBiophys 2003; 417:3-11.
of Inhibition of Mycobacterium avium and Mycobacterium 46. Philip M, Rowley DA, Schreiber H. Inflammation as a tumor
tuberculosis, J Agric Food Chem 1998; 46(7):2504–8. promoter in cancer induction. Semin Cancer Biol 2004; 14:433-9.
22. Srivastava KC. Aqueous extracts of onion, garlic and ginger inhibit 47. Marx J. Inflammation and cancer: the link grows stronger. Science
platelet aggregation and alter arachidonic acid metabolism. Biomed 2004; 306:966-68.
Biochim Acta 1984; 43(8-9):S335-346. 48. Coussens LM, Werb Z. Inflammation and cancer. Nature 2002;
23. Srivastava KC, Mustafa T. Ginger (Zingiber officinale) and rheumatic 420:860-67.
disorders. Med Hypotheses 1989; 29:25–28. 49. Aggarwal BB. Signaling pathways of TNF superfamily: a double-
24. Srivastava KC, Mustafa T. Ginger (Zingiber officinale) in rheumatism and edged sword. National Review Immunology 2003; 3:745-56.
musculoskeletal disorders. Med Hypotheses 1992; 39:342- 348. 50. Aggarwal BB. Nuclear factor-κB: The enemy within. Cancer Cell
25. Afzal M, Al-Hadidi, D Menon, M Pesek, J Dhami MS. Ginger: an 2004; 6:203-08.
ethnomedical, chemical and Pharmacological review. Drug Metab 51. Park KK, Chun KS, Lee SS, Surh YJ. Inhibitory effect of [6] -
Interact 2001; 18:159-190. gingerol, a major pungent principle of ginger, on phorbol ester-
26. Grzanna R, Lindmark L, Frondoza CG. Ginger– an herbal medicinal induced inflammation, epidermal ornithine decarboxylase activity
product with broad anti-inflammatory action. J Med Food 2005; and skin tumor promotion in ICR mice. Cancer Lett 1998; 129:139-
8:125- 132. 44.
27. Jolad SD, Lantz RC, Chen GJ, Bates RB, Timmermann BN. 52. Surh YJ. Cancer chemoprevention with dietary phytochemical.Nat
Commercially processed dry ginger (Zingiber officinale): Rev Cancer 2003; 3:768-80.
composition and effects on LPS-stimulated PGE2 production. 53. Hudson EA, Fox LH, Luckett JCA, Manson MM. Ex vivo cancer
Phytochemistry 2005; 66:1614–35. chemoprevention research possibilities. Environmental Toxicology
28. Lantz RC, Chen GJ, Sarihan M, Solyom AM, Jolad SD, Timmermann and pharmacology 2006; 21:204-14.
BN. The effect of extracts from ginger rhizome on inflammatory 54. Kim SO, Chun KS, Kundu J, Surh YJ. Inhibitory effects pg 6-
mediator production. Phytomedicine 2007; 14:123–8. gingerol on PMA-induced COX-2 expression and activation of NFκB
29. Subodh K, Singh UN, Kiran S, Ravi S. Supplementation of ginger and p38 MAPK in skin mouse. Biofactors 2004; 21:27-31.
with anti-tuberculosis treatment (ATT): A better approach to treat 55. Aggarwal BB, Shishodia S. Molecular targets of dietary for
anemic pulmonary tuberculosis patients. International Journal of prevention and therapy of cancer. Biochem Pharmacol 2006;
Herbal Medicine 2013; 1(3):17-20. 71:1397-21.
30. Jagetia GC, Baliga MS, Venkatesh P, Ulloor JN. Influence of ginger 56. Habib SHM, Makpol S, Hamid NAA, Das S, Ngah WZW, Yusof
rhizome (Zingiber officinale Rosc.) on survival, glutathione and lipid YAM. Ginger extract (Zingiber officinale) has anti-cancer and anti-
peroxidation in mice after whole-body exposure to gamma radiation. inflammatory effects on ethionine-induced hepatoma rats. Clinics
Radiat Res 2003; 160:584–592. 2008; 63:807-13.
31. Haksar A, Sharma A, Chawla R, Kumar R, Arora RS, Prasad S, Gupta 57. Okigbo RN, Mmeka EC. An appraisal of Phytomedicine in Africa.
J, Tripathi M et al. Zingiber officinale exhibits behavioral KMITL Sci Tech J 2006; 6(2):83–94.
radioprotection against radiation 2006; 84: 179–188. 58. Zingiber officinale. The Wealth of India. CSIR Publications and
32. Kim JK, Kim YN, Surh KMYJ, Kim TY. [6]-Gingerol prevents UVB- Information Directorate, New Delhi 1976; 11:102-115.
induced ROS production and COX-2 expression in vitro and in vivo. 59. Acute Phase Reaction and Acute Phase Proteins J. Zhejiang Univ Sci
Free Radic Res 2007; 41:603–614. B 6Nov2005; (11):1054-56.
33. Kiuchi F et al. “Inhibitors of Prostaglandin Biosynthesis from 60. Weiss G, Goodnough LT. Anemia of chronic disease. N Engl J Med
Ginger”, Chemical and pharmaceutical bulletin 1982; 30(2):754-757. 2005; 352:1011-23.
34. Iwakmi S et al. “Inhibition of Arachidonate 5-Lipoxygenase by
Phenolic Compounds”, Chemical and pharmaceutical bulletin 1986;
34(9):3960-3963.
35. WHO Monographs on selected medicinal plants. World Health
Organization, 1999; 1:277-287.
36. AggarwaL BB, Kumar A, Aggarwal MS et al. Curcumin derived from
turmeric (Curcuma longa): a spice for all seasons. In Phytochemicals
in Cancer Chemoprevention. DebasisBagchi PD & Preuss HG, Eds.
CRC Press, New York 2005; 349–387.
37. Shishirshishodia, Gautamsethi, Bharat BA. Curcumin: Getting Back
to the Roots. Ann NY Acad Sci 2005; 1056: 206-217.
38. Tripathi S, Maier KG, Bruch D, Kittur DS; in press. Effect of 6-
gingerol on pro-inflammatory cytokine production and costimulatory
molecule expression in murine peritoneal macrophages. J Surg Res
2007; 138:209-213.
International Journal of Herbal Medicine pada tahun 2013; 1 (4): 16-20
Subodh Kumar
Departemen biokimia, Mayor S
D Singh Medical College & rumah sakit
Kiran Saxena
Departemen biokimia, Chirayu
Medical College & rumah sakit, Bhopal
Uday N. Singh
Ravi Saxena
ABSTRAK
1. Pendahuluan
~ 17 ~
International Journal of Pengobatan Herbal (8-gengerol dan 10 gingerol) adalah lebih aktif, dengan nilai-nilai
MIC 25-50 μg / ml dipamerkan menuju M. TBC H37Rv dan M.
avium [40, 41] .
tuberkulosis pasien dan menyimpulkan bahwa jahe suplementasi
pada pasien tersebut tidak hanya meningkatkan penyerapan besi
tetapi juga signifikan penurunan CRP, feritin dan peningkatan
signifikan
~ 18 ~
International Journal of Pengobatan Herbal penyakit kardiovaskular, Diabetes Tipe 2, kanker, Arthritis,
Alzheimer, penyakit saraf dan penyakit autoimun), dan inhibisi
aktivasi NF-κB dapat menekan peradangan. Atas ekspresi NF-κB,
jahe pada jalur NF-κB: aplikasi topikal dari 6-gingerol COX2, 5-asap, dan iNOS mengarah ke peradangan dan gangguan
menghambat ekspresi TPA-induced COX-2 dan ditekan NF-κB peradangan yang terkait. Karena jahe ampuh NF-κB penghambatan
DNA mengikat kegiatan mice kulit [51, 54] . 6-gingerol dan 6- tindakan, menekan ekspresi COX2, 5-asap, dan iNOS, paling
paradol telah dilaporkan memiliki aktivitas anti-inflamasi yang mungkin melalui downregulation aktivasi NF-κB. Jahe dapat
kuat dan untuk menekan produksi TNF-α diperlakukan TPA- bertindak sebagai anti-inflamasi agen dengan menghalangi aktivasi
perempuan ICR-tikus dan tikus [51, 52]. Menghambat aktivitas NF- NF-κB melalui penindasan sitokin pro-inflamasi, TNF-α. (Fig. 3)
κB, kemudian akan menghambat peradangan dan gangguan
peradangan yang terkait. Senyawa aktif alami di jahe (gingerols
dan zerumbone) telah ditemukan untuk menjadi kuat inhibitor
untuk NF-κB dan sitokin pro-inflamasi TNF-a. Jahe dapat
menghalangi salah satu atau lebih langkah di jalur signaling NF-
κB, seperti sinyal yang mengaktifkan sinyal NF-κB cascade,
translokasi NF-κB ke inti, mengikat DNA dimers atau interaksi
dengan mesin transcriptional basal [55] .
4. referensi
~ 19 ~
International Journal of Pengobatan Herbal 37. Shishirshishodia, Gautamsethi, Bharat BA. Curcumin: Kembali
38. Tripathi S, Kittur Maier KG, Bruch D, DS; di tekan. Efek dari 6-
Agregasi trombosit dan mengubah metabolisme arachidonic acid. gingerol pada produksi sitokin pro-inflamasi dan costimulatory
BioMed BiochimActa 1984; 43(8-9):S335-346. molekul ekspresi di tumore peritoneal makrofag. J Surg Res 2007;
17. Weidner MS, Sigwart K. Keselamatan ekstrak jahe di tikus. J 138:209-213.
Ethnopharmacol 2000; 73: 513-520.
18. Vaes LP, Chyka PA. Interaksi dari warfarin dengan bawang putih, jahe,
ginkgo, atau ginseng: sifat bukti. Ann Pharmacother 2000; 34: 1478 –
1482.
39. Igarashi M, Hayashi C, Homma Y, Hattori S, Kinoshita N, Hamada M,
19. Yamada Y, Kikuzaki H, identifikasi N. Nakatani antimikroba Gingerols
Takeuchi T, J Antibiot 2000; 53:1096.
dari jahe (Zingiber officinale Roscoe), J Antibact Antifung agen 1992;
40. Takeuchi T, Igarashi M, Naganawa H, M. Hamada 2001, JP
20 (6): 309 – 11.
2001055386.
41. Kondo S, Yasui K, Katayama M, Marumo S, Kondo T, Hattori H,
20. GalaL AM. Aktivitas antimikroba 6-paradol dan senyawa terkait, Int. J
Tetrahedron Lett 1987; 28:5861.
Pharmacogn 1996; 34 (1): 64 – 9.
42. Tomas G. molekuler kontrol besi transportasi. J Am Soc Nephrol 2007;
21. Hiserodt RD, Franzblau SG, Rosen RT. isolasi 6-, 8-, 10-Gingerol dari
18:394-400.
jahe Rhizome oleh HPLC dan evaluasi awal inhibisi Mycobacterium
43. TRE JE et al. Respon fase akut dan sistem haematopoietic: peran sitokin.
avium dan Mycobacterium tuberculosis, J Agric Food Chem 1998; 46
Crit Rev Oncol Hemato 1995; 21:1-18.
(7): 2504- 8.
22. Srivastava KC. Aqueous ekstrak bawang merah, bawang putih dan jahe
44. Epstein FH: protein fase akut dan sistemik tanggapan terhadap
menghambat Agregasi trombosit dan mengubah metabolisme peradangan. N Engl J Med 1999; 340:448-454.
arachidonic acid. Acta BioMed Biochim 1984; 43(8-9):S335-346.
45. Ohshima H, Tatemicho M, dasar kimia T. Sawa karsinogenesis
23. Srivastava KC, Mustafa T. jahe (Zingiber officinale) dan gangguan peradangan yang disebabkan. Arch. BiochemBiophys 2003; 417:3-
rematik. Med hipotesis 1989; 29:25 – 28.
11.
24. Srivastava KC, Mustafa T. jahe (Zingiber officinale) di rematik dan
46. Philip M, Rowley DA, peradangan H. Schreiber sebagai tumor
gangguan muskuloskeletal. Med hipotesis 1992; 39:342-348.
promotor di induksi kanker. Berbagai kanker Semin 2004; 14:433-9.
47. Marx J. peradangan dan kanker: link tumbuh lebih kuat. Ilmu 2004;
25. M Afzal, Al-Hadidi, D Menon, M Pesek, J Dhami MS. jahe:
306:966-68.
ethnomedical, kimia dan farmakologis review. Obat Metab
48. Coussens LM, Werb Z. peradangan dan kanker. Alam 2002; 420:860-
berinteraksi 2001; 18:159-190.
67.
26. Grzanna R, Lindmark L, Frondoza CG. Jahe-produk obat herbal
49. Aggarwal BB. Menandakan jalur TNF superfamili: pedang bermata
dengan luas tindakan anti-inflamasi. Makanan Med J 2005; 8:125-
dua. National Review imunologi 2003; 3:745-56.
132.
50. Aggarwal BB. Faktor-κB nuklir: musuh dalam. Sel kanker 2004;
27. SD Jolad, Lantz RC, Chen GJ, Bates RB, Timmermann BN. diproses
6:203-08.
secara komersial kering jahe (Zingiber officinale): komposisi dan efek
51. Park KK, Chun KS, Lee SS, Surh YJ. Efek penghambatan [6] -
pada produksi PGE2 dirangsang LPS. Fitokimia 2005; 66:1614 – 35.
gingerol, prinsip utama yang pedas dari jahe, phorbol ester yang
disebabkan peradangan, epidermal ornithine dekarboksilase kegiatan
28. Lantz RC, Chen GJ, Sarihan M, Solyom AM, Jolad SD, Timmermann
dan promosi tumor kulit pada tikus ICR. Kanker Lett 1998; 129:139-
BN. Efek ekstrak dari rimpang jahe di produksi mediator inflamasi.
44.
Phytomedicine 2007; 14:123 – 8.
52. Surh YJ. Cancer chemoprevention dengan diet fitokimia. NAT Rev
29. Subodh K, PBB Singh, Kiran S, Ravi S. suplementasi jahe dengan
kanker 2003; 3:768-80.
pengobatan anti-tuberkulosis (ATT): pendekatan yang lebih baik
53. Hudson EA, Fox LH, Luckett JCA, Manson MM. Ex vivo cancer
untuk mengobati pasien anemia TBC paru-paru. International Journal
chemoprevention penelitian kemungkinan. Lingkungan Toksikologi
of Herbal Medicine pada tahun 2013; 1 (3): 17-20.
dan Farmakologi 2006; 21:204-14.
30. Jagetia GC, Baliga MS, Venkatesh P, Yohanes Ulloor Pengaruh
54. Kim Jadi, Chun KS, Kundu J, Surh YJ. Efek penghambatan pg 6-
rimpang jahe (Zingiber officinale (Rosc.) pada kelangsungan hidup,
gingerol PMA-induced COX-2 ekspresi dan aktivasi NFκB dan p38
glutathione dan lipid peroxidation pada tikus setelah paparan radiasi
MAPK di kulit mouse. Biofactors tahun 2004; 21:27-31.
gamma seluruh tubuh. Radiat Res 2003; 160:584-592.
55. Aggarwal BB, Shishodia S. molekuler target dari diet untuk
31. Haksar A, Sharma A, Chawla R, Kumar R, Arora RS, Prasad S, Gupta
pencegahan dan terapi kanker. Biochem Pharmacol 2006; 71:1397-
J, Tripathi M et al. Zingiber officinale pameran perilaku
21.
radioprotection terhadap radiasi 2006; 84: 179-188.
56. Habib SHM, Makpol S, Hamid NAA, Das S, Ngah WZW, Yusof YAM.
32. Kim JK, Kim YN, Surh KMYJ, Kim TY. [6]-Gingerol mencegah
Ekstrak jahe (Zingiber officinale) memiliki efek anti kanker dan anti-
diinduksi UVB ROS produksi dan ekspresi COX-2 secara in vitro dan
inflamasi pada tikus hepatoma diinduksi ethionine. Klinik 2008;
in vivo. Gratis Radic Res 2007; 41:603-614.
63:807-13.
33. Kiuchi F et al. "Inhibitor biosintesis Prostaglandin dari jahe", kimia
57. Okigbo RN, Mmeka EC. Sebuah penilaian dari Phytomedicine di
dan farmasi buletin 1982; 30 (2): 754-757.
Afrika. KMITL Sains teknologi J 2006; 6 (2): 83 – 94.
34. Iwakmi S et al. "Penghambatan Arachidonate 5-Lipoxygenase oleh 58. Zingiber officinale . Kekayaan India. CSIR publikasi dan Direktorat
senyawa fenolik", kimia dan farmasi buletin 1986; 34 (9): 3960-3963. informasi, New Delhi 1976; 11:102-115.
59. Reaksi fase akut dan protein fase akut J. Zhejiang Univ Sci B 6 Nov
35. Yang monograf pada tanaman obat yang dipilih. Organisasi Kesehatan
2005; (11): 1054-56.
Dunia, 1999; 1:277-287.
60. G Weiss, Goodnough LT. Anemia kronis penyakit. N Engl J Med 2005;
36. AggarwaL BB, Kumar A, Aggarwal MS et al. Curcumin berasal dari
kunyit (Curcuma longa): rempah-rempah untuk semua musim. 352:1011-23.
Dalam Phytochemical dalam Chemoprevention kanker.
DebasisBagchi PD & Preuss HG, Eds. CRC Press, New York tahun
2005; 349-387.
~ 20 ~
~ 20 ~