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Ginger

Botanical Name: Zingiber officinale Roscoe.
Pharmacopoeial Name: Zingeribis rhizoma.
Synonym: Amomum zingiber L.
Common Names: Ginger, zingiber.

Summary Table
herb description

Family

Zingiberaceae.

Habitat and Cultivation

Perennial, with tuberous rhizomes, native to Southeast Asia, and cultivated in tropical regions, including India, West Indies, Jamaica, Africa, and China.

Parts Used

Rhizome.

Common Forms

  • Fresh or Dried Rhizome:   considered different agents in Chinese practice.

Dried Powdered Rhizome.

Tincture (1:5), Fluid Extract (1:1), 90% ethanol, fresh or dried rhizome.

  • Standardized Extracts:   Various, including EV.EXT 33 (Ferrosan) standardized to hydroxy-methoxy phenols; Zintona standardized to 1.4% volatiles and minimum of 2.0 mg gingerols and shogoals per 250-mg capsule.

herb in clinical practice

Overview

Best known as a pungent spice and dietary ingredient, ginger is among the top-20 dietary supplements in retail sales in the United States. Primarily viewed by conventional medicine as an antiemetic for motion sickness, the nausea of pregnancy, and postoperative nausea, the herb has many more, diverse therapeutic applications in both Western and Asian botanical medicine. It has potent anti-inflammatory effects on eicosanoid metabolism, circulatory and digestive tonic actions, and metabolic, endocrine, antimicrobial, antipyretic, antioxidant, and antineoplastic activities. Toxicity is minimal, and ginger is free of adverse effects at therapeutic doses.

Therapeutic monographs for ginger generally limit the indications to recent clinical trial–driven applications. Ginger was approved by the German Commission E in 1988 for dyspepsia and motion sickness, although not for morning sickness. 1 The European Scientific Cooperative on Phytotherapy (ESCOP) 2 recently reviewed much of the research but also suggested only motion sickness and postoperative nausea prevention as clinical uses. Broader authoritative surveys of the herb can be found in literature reviews by Mills and Bone 3 and McKenna et al. 4 Recent interest in the cancer chemopreventive properties has provided a new emphasis in pharmacological research into ginger and its constituent compounds. 5,6

Historical/Ethnomedicine Precedent

Ginger has been used for centuries in Ayurvedic and Chinese medicine, where it is a major ingredient in innumerable formulae for many treatment indications. In India, ginger is not only widely used as a spice and meat preservative and antimicrobial digestive tonic, but also considered to have aphrodisiac and cognitive-enhancing effects, especially on memory, and has also been used as a narcotic antagonist. In classical Chinese medicine, the fresh rhizome (Sheng Jiang) is distinguished from the dried and processed rhizome (Gan Jiang) . In light of modern precautions suggesting elevated risk of bleeding with ginger consumption, an interesting Chinese medical use of dried ginger is to arrest bleeding, especially bleeding associated with “Deficiency” and “Cold.” 7 Doses of the herb in Chinese practice are considerably higher than in modern phytotherapy, maximum dosage for Sheng Jiang is 30 g. 7 Traditional Western botanical medicine considers ginger to be a “diffusive stimulant,” to be added to formulae to enhance the bioavailability of other herbs, as well to support diffusive physiological processes (e.g., expectoration, diaphoresis). 3

Known or Potential Therapeutic Uses

Appetite stimulation, dyspepsia, flatulence, digestive/choleretic secretory stimulation, increasing bioavailability of foods and medicines, ulceroprotection, circulatory stimulation, thermogenesis, menstrual flow irregularities, colds, influenza, fevers, atherosclerosis, hypercholesterolemia, hyperviscosity, hepatic protection, pain relief in osteoarthritis and rheumatoid arthritis, Kawasaki's disease, antiemesis in nausea of motion, pregnancy, drug withdrawal, and chemotherapy; antineoplastic adjuvant.

Key Constituents

Pungent oleoresin containing phenolic gingerols and their dehydration derivatives, shogoals (formed by drying); volatile oil (variable composition of monoterpenes and sesquiterpenes depending on botanical chemotypes and physical methods of preparation).

Therapeutic Dosing Range

  • Fresh or Dried Rhizome: 2 to 4 g daily.
  • Tincture 1:5 (90% ethanol): 1.25 to 3.0 mL three times daily.
  • Fluid Extract 1:1 (90% ethanol): 0.25 to 0.75 mL three times daily.
  • Standardized Extract: Dose equivalent to 2 to 4 g dried rhizome daily.

interactions review

Strategic Considerations

The available therapeutic monographs on ginger minimize suggestions of herb-drug interactivity. The German Commission E listed ginger interactions under “none known,” 1 ESCOP 2 mentions only the possible increase in bioavailability of sulfaguanide, and the World Health Organization (WHO) 8 monograph suggests an “enhancement” of pharmaceutical anticoagulant therapy, adding that the clinical significance of the possible interaction has not been evaluated. By contrast, secondary literature and commentators in both professional and popular press emphasize potential anticoagulant effects of ginger and freely extrapolate to hypothetical interactions with drugs affecting hemostasis.

The presumed mechanism of interference with normal hemostasis by ginger is based on in vitro studies that suggest the herb may affect platelet aggregation, primarily through inhibition of eicosanoid metabolism and specifically reduction of thromboxane levels. 9 However, the experimental support is inconclusive, and to date the balance of in vivo studies suggest a lack of effect of ginger on thromboxane-induced platelet aggregation in humans. 10-15Until recently, clinical reports were based only on a questionable single case report of platelet aggregation inhibition apparently attributed to the consumption of ginger marmalade. 16 A recent single report of elevated international normalized ratio (INR) and epistaxis in a patient previously stable on phenprocoumon anticoagulant therapy is discussed later. 17 However, no pharmacological data show that ginger affects the coagulation pathways reflected by the INR, so this case remains an isolated and unexplained interaction, its significance unclear. The existence of only two somewhat controversial reports in a quarter century suggests that portentous warnings about risks of combining ginger with anticoagulants may be overstated.

The activity of the herb as an anti-inflammatory, analgesic, and circulatory stimulant has led to its incorporation in protocols for arthritis. Coadministration of ginger in combination regimens with nonsteroidal anti-inflammatory drugs (NSAIDs) or analgesics for arthritis has been examined indirectly in trials that permitted NSAID/analgesic rescue or in one trial where patients added ginger to an existing NSAID regimen. 18-20Although further investigations are warranted, there may be neither significant additive effect between NSAIDs and ginger alone in arthritis nor any significant difference between NSAIDs and ginger alone for arthritic symptom relief. However, ginger's adverse effect profile is superior to conventional NSAID drugs, and ginger could be incorporated into combination protocols for botanical cyclooxygenase-2 (COX-2) inhibition in arthritis and related inflammatory conditions to maintain integrity of the protective, constitutive gastric cyclooxygenase and prostaglandin E2(PGE2). Common compound formulations with ginger include herbs such as rosemary, Boswellia, and the plant-derived compound resveratrol, which act as COX-2 inhibitors at the receptor level and also downregulate inducible COX-2 transcription. Ginger extracts have been shown to exert an ulceroprotective effect against aspirin and indomethacin, implying the pharmacology of ginger-containing combination protocols targeting COX-2 could be applied to a variety of inflammatory conditions, including malignancy. 21

The established antiemetic effects of ginger, well proven for motion sickness and morning sickness of pregnancy, have also been found to be helpful in drug-induced nausea and vomiting. The strong association of certain antineoplastic chemotherapies (e.g., cisplatin) with acute nausea, as well as postoperative nausea and vomiting (PONV) associated with emetogenic anesthetics, constitute beneficial interactions with ginger (see anesthetics and chemotherapies later). Ginger may well find application in the treatment of other cases of drug-induced nausea when symptom occurrence is not inevitable; one report suggests that it can be used for nausea relating to symptoms of disequilibrium after discontinuation of serotonin-inhibiting drugs. 22

Effects on Drug Metabolism and Bioavailability

An experimental study found that ginger enhanced the absorption of sulfaguanidine across the small intestine in rodents. 23 Secretory increases by the pancreas and bile are also associated with ginger administration. 24 An early study suggests glucuronide conjugation and renal and biliary excretion are involved in elimination of the volatile component zingerone. 25 In rats, [6]-gingerol was eliminated partly by hepatic metabolism, and the gingerol was more than 90% bound to serum protein. 26

Traditionally, ginger has been used to promote the absorption of herbs in multiherb botanical prescriptions. The Ayurvedic Trikatu formula is a mixture of ginger with long-pepper and black pepper that has been shown to increase the bioavailability of several pharmaceuticals. 27 A more recent study of the effect of Trikatu on the kinetics of sodium diclofenac found the opposite effect: a significant reduction of bioavailability. 28 These studies are not applicable directly to ginger alone, and the piperine ingredient of the other herbs in the formula are known to have modulating effects on several cytochrome P450 isoforms. 29

Data on potential effects of ginger and its constituents on drug-metabolizing enzymes are largely unavailable at this time. Although traditional botanical prescribing conventions may use ginger for increasing bioavailability of other herbs, the effects on pharmaceutical drug absorption are not predictable on the basis of the current data. One study has documented an inhibitory effect on P-glycoprotein (P-gp). Accumulation of daunorubicin was increased in a multidrug-resistant cell line in the presence of [6]-gingerol, which also appeared to increase the cytotoxicity of vinblastine, suggesting an inhibition of P-gp–mediated efflux of the cytotoxic drug from the cells. 30 Until further data are available, the prediction of P-gp–mediated drug-ginger interactions remains speculative, if theoretically possible.

herb-drug interactions
Anesthesia, General
Antiplatelet Agents
Cisplatin and Emetogenic Antineoplastic Chemotherapies
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) and Analgesic Antiarthritics
  • COX-1 inhibitors:Diclofenac (Cataflam, Voltaren), combination drug: diclofenac and misoprostol (Arthrotec), diflunisal (Dolobid), etodolac (Lodine), fenoprofen (Dalfon), furbiprofen (Ansaid), ibuprofen (Advil, Excedrin IB, Motrin, Motrin IB, Nuprin, Pedia Care Fever Drops, Provel, Rufen); combination drug: hydrocodone and ibuprofen (Reprexain, Vicoprofen); indomethacin (indometacin; Indocin, Indocin-SR), ketoprofen (Orudis, Oruvail), ketorolac (Acular ophthalmic, Toradol), meclofenamate (Meclomen), mefenamic acid (Ponstel), meloxicam (Mobic), nabumetone (Relafen), naproxen (Aleve, Anaprox, Naprosyn), oxaprozin (Daypro), piroxicam (Feldene), salsalate (salicylic acid; Amigesic, Disalcid, Marthritic, Mono Gesic, Salflex, Salsitab), sulindac (Clinoril), tolmetin (Tolectin).
  • COX-2 inhibitors:Celecoxib (Celebrex).
Beneficial or Supportive Interaction, Not Requiring Professional Management
Prevention or Reduction of Drug Adverse Effect

Probability: 2. Probable
Evidence Base: Preliminary

Effect and Mechanism of Action

Ginger and ginger extracts exert anti-inflammatory effects through multiple mechanisms, including cyclooxygenase and lipoxygenase inhibition. Adjuvant combination of ginger with NSAIDs for arthritis leads to increased symptom relief and allows the NSAID dose to be lowered and in some cases discontinued. Ginger has a superior adverse effect profile to known NSAIDs, and coadministration reduces adverse effects through lower NSAID dose or eventual substitution.

Research

In vitro evidence has established that ginger and some of its constituent compounds are effective inhibitors of cyclooxygenase and lipoxygenase and may downregulate transcription of cyclooxygenase and inducible nitric oxide synthase (iNOS) by inhibition of NF-κB. 21,42-44 Two randomized placebo-controlled clinical trials have demonstrated small but significant effects for ginger treatment of osteoarthritis, although in the study by Bliddal et al. 19 the effect was small compared with ibuprofen and was confined to a first period of treatment in a crossover design. The trial by Altman and Marcussen 20 showed a significant effect in 261 patients with osteoarthritis of the knee, although the ginger extract was administered in combination with the herb galangal (Alpinia galangia). Acetaminophen was permitted as a rescue medication in both studies. The ginger group had less use of rescue medication than the placebo group. Additionally, several rodent experimental model studies have shown that ginger extracts are directly protective against NSAID-induced gastric ulcers in a rodent model. 55-58

Reports

Srivastafa and Mustafa 59 reported a case series of seven patients who used ginger extracts combined with NSAIDs, but who were not taking other antiarthritic medications (e.g., gold) or steroids. Six patients were taking NSAIDs for 3 months but failed to experience symptom relief. After 3 months of oral ginger administration (up to 5.0 g fresh rhizome or 1.0 g powdered rhizome daily), while continuing NSAID therapy, the patients all experienced reduction in pain symptoms and improved range of motion, and two patients also experienced relief of myalgia. After 3 months of coadministration the NSAIDs were stopped; the patients continued with ginger alone and were able to maintain the same degree of symptom relief.

Integrative Therapeutics, Clinical Concerns, and Adaptations

The adverse effect profile of NSAIDs, including the COX-2 specific inhibitors, continues to present significant problems to the pharmaceutical anti-inflammatory strategies for arthritis. Ginger extracts may additively combine with NSAIDs and after a period of coadministration can substitute for them in some cases. Health care professionals versed in botanical medicine are more likely to incorporate ginger into polyherbal anti-inflammatory formulae rather than use it as a single agent. Typical associated ingredients might include curcumin, Boswellia serrata,resveratrol, and the salicylate-containing Salixspp.

Phenprocoumon and Related Oral Vitamin K Antagonist Anticoagulants
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Aminoglycoside Antibiotics
Sulfaguanidine
Citations
  • 1.Blumenthal M, Busse W, Goldberg A et al. The Complete German Commission E Monographs. Austin, Texas: American Botanical Council: Integrative Medicine Communications; 1998.
  • 2.ESCOP. Zingiberis Rhizoma. ESCOP Monographs: the Scientific Foundation for Herbal Medicinal Products. 2nd ed. Exeter, UK: European Scientific Cooperative on Phytotherapy and Thieme; 2003:547-553.
  • 3.Mills S, Bone K. Principles and Practice of Phytotherapy. Edinburgh: Churchill Livingstone; 2000.
  • 4.McKenna D, Jones K, Hughes K, Humphrey S. Ginger. Botanical Medicines. 2nd ed. Binghamton, NY: Haworth Press; 2002:223-254.
  • 5.Aggarwal BB, Shishodia S. Molecular targets of dietary agents for prevention and therapy of cancer. Biochem Pharmacol 2006;71:1397-1421.View Abstract
  • 6.Aggarwal BB, Takada Y, Oommen OV. From chemoprevention to chemotherapy: common targets and common goals. Expert Opin Invest Drugs 2004;13:1327-1338.View Abstract
  • 7.Chen J, Chen T. Chinese Medical Herbology and Pharmacology. City of Industry, Calif: Art of Medicine Press Inc; 2004.
  • 8.WHO. Rhizoma Gingeribis. WHO Monographs on Selected Medicinal Plants. 1 vol. Geneva: World Health Organization; 1999:277-287.
  • 9.Backon J. Ginger: inhibition of thromboxane synthetase and stimulation of prostacyclin: relevance for medicine and psychiatry. Med Hypotheses 1986;20:271-278.View Abstract
  • 10.Srivastava KC. Effect of onion and ginger consumption on platelet thromboxane production in humans. Prostaglandins Leukot Essent Fatty Acids 1989;35:183-185.View Abstract
  • 11.Bordia A, Verma SK, Srivastava KC. Effect of ginger (Zingiber officinale Rosc.) and fenugreek (Trigonella foenumgraecum L.) on blood lipids, blood sugar and platelet aggregation in patients with coronary artery disease. Prostaglandins Leukot Essent Fatty Acids 1997;56:379-384.View Abstract
  • 12.Lumb AB. Effect of dried ginger on human platelet function. Thromb Haemost 1994;71:110-111.View Abstract
  • 13.Janssen PL, Meyboom S, van Staveren WA et al. Consumption of ginger (Zingiber officinale roscoe) does not affect ex vivo platelet thromboxane production in humans. Eur J Clin Nutr 1996;50:772-774.
  • 14.Srivastava KC. Aqueous extracts of onion, garlic and ginger inhibit platelet aggregation and alter arachidonic acid metabolism. Biomed Biochim Acta 1984;43:S335-346.View Abstract
  • 15.Guh JH, Ko FN, Jong TT, Teng CM. Antiplatelet effect of gingerol isolated from Zingiber officinale. J Pharm Pharmacol 1995;47:329-332.View Abstract
  • 16.Dorso CR, Levin RI, Eldor A et al. Chinese food and platelets. N Engl J Med 1980;303:756-757.View Abstract
  • 17.Krüth P, Brosi E, Fux R et al. Ginger-associated overanticoagulation by phenprocoumon. Ann Pharmacother 2004;38:257-260.
  • 18.Srivastava KC, Mustafa T. Ginger (Zingiber officinale) in rheumatism and musculoskeletal disorders. Med Hypotheses 1992;39:342-348.View Abstract
  • 19.Bliddal H, Rosetzsky A, Schlichting P et al. A randomized, placebo-controlled, cross-over study of ginger extracts and ibuprofen in osteoarthritis. Osteoarthritis Cartilage 2000;8:9-12.View Abstract
  • 20.Altman RD, Marcussen KC. Effects of a ginger extract on knee pain in patients with osteoarthritis. Arthritis Rheum 2001;44:2531-2538.View Abstract
  • 21.Surh YJ, Chun KS, Cha HH et al. Molecular mechanisms underlying chemopreventive activities of anti-inflammatory phytochemicals: down-regulation of COX-2 and iNOS through suppression of NF-kappa B activation. Mutat Res 2001;480-481:243-268.View Abstract
  • 22.Schechter JO. Treatment of disequilibrium and nausea in the SRI discontinuation syndrome. J Clin Psychiatry 1998;59:431-432.View Abstract
  • 23.Sakai K, Oshima N, Kutsuna T et al. [Pharmaceutical studies on crude drugs. I. Effect of the Zingiberaceae crude drug extracts on sulfaguanidine absorption from rat small intestine]. Yakugaku Zasshi 1986;106:947-950.View Abstract
  • 24.Platel K, Rao A, Saraswathi G, Srinivasan K. Digestive stimulant action of three Indian spice mixes in experimental rats. Nahrung 2002;46:394-398.View Abstract
  • 25.Monge P, Scheline R, Solheim E. The metabolism of zingerone, a pungent principle of ginger. Xenobiotica 1976;6:411-423.View Abstract
  • 26.Naora K, Ding G, Hayashibara M et al. Pharmacokinetics of [6]-gingerol after intravenous administration in rats with acute renal or hepatic failure. Chem Pharm Bull (Tokyo) 1992;40:1295-1298.View Abstract
  • 27.Atal CK, Zutshi U, Rao PG. Scientific evidence on the role of Ayurvedic herbals on bioavailability of drugs. J Ethnopharmacol 1981;4:229-232.View Abstract
  • 28.Lala LG, D’Mello PM, Naik SR. Pharmacokinetic and pharmacodynamic studies on interaction of “Trikatu” with diclofenac sodium. J Ethnopharmacol 2004;91:277-280.
  • 29.Zhou S, Gao Y, Jiang W et al. Interactions of herbs with cytochrome P450. Drug Metab Rev 2003;35:35-98.View Abstract
  • 30.Nabekura T, Kamiyama S, Kitagawa S. Effects of dietary chemopreventive phytochemicals on P-glycoprotein function. Biochem Biophys Res Commun 2005;327:866-870.View Abstract
  • 31.Bone ME, Wilkinson DJ, Young JR et al. Ginger root—a new antiemetic: the effect of ginger root on postoperative nausea and vomiting after major gynaecological surgery. Anaesthesia 1990;45:669-671.View Abstract
  • 32.Arfeen Z, Owen H, Plummer JL et al. A double-blind randomized controlled trial of ginger for the prevention of postoperative nausea and vomiting. Anaesth Intensive Care 1995;23:449-452.View Abstract
  • 33.Eberhart LH, Mayer R, Betz O et al. Ginger does not prevent postoperative nausea and vomiting after laparoscopic surgery. Anesth Analg 2003;96:995-998, table of contents.
  • 34.Pongrojpaw D, Chiamchanya C. The efficacy of ginger in prevention of post-operative nausea and vomiting after outpatient gynecological laparoscopy. J Med Assoc Thai 2003;86:244-250.View Abstract
  • 35.Visalyaputra S, Petchpaisit N, Somcharoen K, Choavaratana R. The efficacy of ginger root in the prevention of postoperative nausea and vomiting after outpatient gynaecological laparoscopy. Anaesthesia 1998;53:506-510.View Abstract
  • 36.Phillips S, Ruggier R, Hutchinson SE. Zingiber officinale (ginger): an antiemetic for day case surgery. Anaesthesia 1993;48:715-717.View Abstract
  • 37.Ernst E, Pittler MH. Efficacy of ginger for nausea and vomiting: a systematic review of randomized clinical trials. Br J Anaesth 2000;84:367-371.View Abstract
  • 38.Morin AM, Betz O, Kranke P et al. [Is ginger a relevant antiemetic for postoperative nausea and vomiting?]. Anasthesiol Intensivmed Notfallmed Schmerzther 2004;39:281-285.View Abstract
  • 39.Chaiyakunapruk N, Kitikannakorn N, Nathisuwan S et al. The efficacy of ginger for the prevention of postoperative nausea and vomiting: a meta-analysis. Am J Obstet Gynecol 2006;194:95-99.View Abstract
  • 40.Suekawa M, Ishige A, Yuasa K et al. Pharmacological studies on ginger. I. Pharmacological actions of pungent constituents, (6)-gingerol and (6)-shogaol. J Pharmacobiodyn 1984;7:836-848.View Abstract
  • 41.Flynn DL, Rafferty MF, Boctor AM. Inhibition of human neutrophil 5-lipoxygenase activity by gingerdione, shogaol, capsaicin and related pungent compounds. Prostaglandins Leukot Med 1986;24:195-198.View Abstract
  • 42.Tjendraputra E, Tran VH, Liu-Brennan D et al. Effect of ginger constituents and synthetic analogues on cyclooxygenase-2 enzyme in intact cells. Bioorg Chem 2001;29:156-163.View Abstract
  • 43.Nurtjahja-Tjendraputra E, Ammit AJ, Roufogalis BD et al. Effective anti-platelet and COX-1 enzyme inhibitors from pungent constituents of ginger. Thromb Res 2003;111:259-265.View Abstract
  • 44.Kim SO, Kundu JK, Shin YK et al. [6]-Gingerol inhibits COX-2 expression by blocking the activation of p38 MAP kinase and NF-κB in phorbol ester-stimulated mouse skin. Oncogene 2005;24:2558-2567.View Abstract
  • 45.Verma SK, Singh J, Khamesra R, Bordia A. Effect of ginger on platelet aggregation in man. Indian J Med Res 1993;98:240-242.View Abstract
  • 46.Jiang X, Williams KM, Liauw WS et al. Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Br J Clin Pharmacol 2005;59:425-432.View Abstract
  • 47.Morrow GR. Susceptibility to motion sickness and chemotherapy-induced side-effects. Lancet 1984;1:390-391.View Abstract
  • 48.Sharma SS, Gupta YK. Reversal of cisplatin-induced delay in gastric emptying in rats by ginger (Zingiber officinale). J Ethnopharmacol 1998;62:49-55.View Abstract
  • 49.Sharma SS, Kochupillai V, Gupta SK et al. Antiemetic efficacy of ginger (Zingiber officinale) against cisplatin-induced emesis in dogs. J Ethnopharmacol 1997;57:93-96.View Abstract
  • 50.Yamahara J, Rong HQ, Naitoh Y et al. Inhibition of cytotoxic drug-induced vomiting in suncus by a ginger constituent. J Ethnopharmacol 1989;27:353-355.View Abstract
  • 51.Abdel-Aziz H, Windeck T, Ploch M, Verspohl EJ. Mode of action of gingerols and shogaols on 5-HT3 receptors: binding studies, cation uptake by the receptor channel and contraction of isolated guinea-pig ileum. Eur J Pharmacol 2006;530:136-143.View Abstract
  • 52.Sharma A, Haksar A, Chawla R et al. Zingiber officinale Rosc. modulates gamma radiation–induced conditioned taste aversion. Pharmacol Biochem Behav 2005;81:864-870.View Abstract
  • 53.Hesketh PJ, Van Belle S, Aapro M et al. Differential involvement of neurotransmitters through the time course of cisplatin-induced emesis as revealed by therapy with specific receptor antagonists. Eur J Cancer 2003;39:1074-1080.View Abstract
  • 54.Mahesh R, Perumal RV, Pandi PV. Cancer chemotherapy-induced nausea and vomiting: role of mediators, development of drugs and treatment methods. Pharmazie 2005;60:83-96.View Abstract
  • 55. Al-Yahya MA, Rafatullah S, Mossa JS et al. Gastroprotective activity of ginger, Zingiber officinale rosc., in albino rats. Am J Chin Med 1989;17:51-56.View Abstract
  • 56.Yamahara J, Mochizuki M, Rong HQ et al. The anti-ulcer effect in rats of ginger constituents. J Ethnopharmacol 1988;23:299-304.View Abstract
  • 57.Yamahara J, Hatakeyama S, Taniguchi K et al. [Stomachic principles in ginger. II. Pungent and anti-ulcer effects of low polar constituents isolated from ginger, the dried rhizoma of Zingiber officinale Roscoe, cultivated in Taiwan. The absolute stereostructure of a new diarylheptanoid]. Yakugaku Zasshi 1992;112:645-655.View Abstract
  • 58.Yoshikawa M, Yamaguchi S, Kunimi K et al. Stomachic principles in ginger. III. An anti-ulcer principle, 6-gingesulfonic acid, and three monoacyldigalactosylglycerols, gingerglycolipids A, B, and C, from Zingiberis Rhizoma originating in Taiwan. Chem Pharm Bull (Tokyo) 1994;42:1226-1230.View Abstract
  • 59.Srivastava KC, Mustafa T. Ginger (Zingiber officinale) and rheumatic disorders. Med Hypotheses 1989;29:25-28.View Abstract
  • 60.Weidener MS, Sigwart K. The safety of a ginger extract in the rat. J Ethnopharmacol 2000;73:513-520.
  • 61.Nagoshi C, Shiota S, Kuroda T et al. Synergistic effect of [10]-gingerol and aminoglycosides against vancomycin-resistant enterococci (VRE). Biol Pharm Bull 2006;29:443-447.View Abstract
  • 62.Corrigan D. Zingiber officinale. In: Smet PD, ed. Adverse Effects of Herbal Drugs. 3 vol. Berlin: Springer; 1997:215-228.