InteractionsGuide Index Page

Case Analysis Toolclose
Enter Each Substance:

Analysis Search Terms:


Botanical Name: Curcuma longa L.
Pharmacopoeial Name: Curcumae longae rhizome.
Synonym: Curcuma domestica Valeton.
Common Names: Turmeric, Indian saffron.

Summary Table
herb description



Related Species

Curcuma aromatica Salisbury, Curcuma xanthorrhiza Roxb.

Habitat and Cultivation

Native to tropical zones in India and Southeast Asia; cultivated for culinary and medicinal purposes for many centuries; now imported principally from India, China, and Indonesia.

Parts Used


Common Forms

  • Dried:   Rhizome, powdered.

Oleoresin or essential oil.

  • Tincture, Fluid Extract:   Dried or fresh rhizome, 45% ethanol.

  • Standardized Extract:   Solid extracts, concentrated and standardized to 95% curcuminoids, as curcumin.

Note: Experimental studies often use purified laboratory-grade diferuloylmethane or curcumin-I only; semisynthetic derivatives are also available.

herb in clinical practice


Although in medicinal use in Asia for more than a millennium, turmeric is probably better known in the West as a common yellow spice from the ginger family, used as a pungent flavoring ingredient in curries, which is also widely used in the U.S. food industry as a coloring agent. Until recently, Western medicine viewed turmeric primarily as a spice with minor aromatic digestive stimulant and hepatic stimulant properties, indicated but little used for functional hepatobiliary disorders. In 1985 the German Commission E approved “Turmeric Root” for dyspeptic conditions, 1 although the herb was absent from both the 1983 and the 1996 edition of the British Herbal Pharmacopoeia . The World Health Organization (WHO) monograph repeats the Commission E indications. 2

Pharmacological investigations into the anticancer and anti-inflammatory properties of the herb and its constituents began to attract research interest in the 1980s. Currently, curcumin is regarded as a natural compound of great interest and of considerable therapeutic potential because of its multiple properties, which include antioxidant, anti-inflammatory, chemopreventive, antimutagenic, anticarcinogenic, antimetastatic, antiangiogenic, and cardioprotective activities. Although this research currently constitutes a rapidly expanding body of literature, a 2003 therapeutic monograph on turmeric by the European Scientific Cooperative on Phytotherapy (ESCOP) 3 echoes the original 1985 Commission E indications for “symptomatic treatment of mild digestive disturbances and minor biliary dysfunction.” Aggarwal et al. 4 recently reviewed the chemopreventive and anticancer molecular biology of curcumin. The majority of recent scientific studies on turmeric employed purified laboratory-grade diferuloylmethane or curcumin-I, which should be noted before extrapolating to mixtures of curcuminoids or to crude whole-herb extracts.

Historical/Ethnomedicine Precedent

In Ayurveda, turmeric is used internally for digestive problems and is considered a blood purifier and antimicrobial. Externally it is used for skin problems, as well as for sprains and strains. The powdered herb is often administered in a base of dietary ingredients, such as milk or honey, or in slaked lime for topical applications. 5 In classical Chinese medicine, turmeric invigorates the xue (blood) and relieves pain, especially related to liver (Gan); it clears heat and cools the blood, clears the heart (Xin) (which helps with psychological problems), and benefits the gallbladder (Dan) and treats jaundice. 6

Known or Potential Therapeutic Uses

Abdominal pain, adjunctive cancer treatment, antimicrobial, arthritis, cardiovascular disease prophylaxis, chemoprevention, chemosensitization, cholestasis, dyspepsia, ethanol-related hepatic conditions, hyperlipidemia, inflammation, jaundice, radiosensitization.

Topically for skin conditions, sprains, and strains.

Key Constituents

Curcuminoids (diferuloylmethanes), including curcumin and its methoxylated derivatives (2%-5%), are the yellow pigments and principal actives. Sometimes designated as curcumins I to IV: I, curcumin; II, desmethoxycurcumin; III, bisdesmethoxycurcumin; and IV, cyclocurcumin.

Essential oil (3% and 5%), including sesquiterpene ketones and monoterpenes.

Therapeutic Dosing Range

  • Powdered Rhizome:   Up to 12 g daily by decoction.

  • Tincture, Fluid Extract:   5 to 15 mL daily (as 1:1 equivalent).

  • Standardized Extract:   Equivalent of 400 to 600 mg curcumin three times daily.

interactions review

Strategic Considerations

No interactions with prescription drugs are noted in the available therapeutic monographs on turmeric. Both Western and Chinese herbal authorities have advised using caution when coadministering turmeric with antiplatelet or anticoagulant drugs and avoiding higher doses of the herb in such settings. 7,8No interaction with anticoagulant or antiplatelet medications has been reported clinically or described experimentally, and the suggested interaction is classified here as “overstated/speculative” (see Theoretical, Speculative, and Preliminary Interactions Research).

The primary clinical context for current use of curcumin extracts is inflammatory conditions and the integrative oncology setting. Curcumin has innumerable effects on a wide range of signal transduction pathways and molecular targets affecting cell growth, multiplication, differentiation, and apoptosis, including inhibition of nuclear factor kappa B (NF-κB) and activating protein-1 (AP-1). 4,9-13Experimental evidence is emerging for potential interactions with a variety of cytotoxic drugs, as well as radiotherapy. A novel interactions issue, unaddressed by research to date, is how curcumin, known to inhibit a number of molecular targets involved in angiogenesis, including vascular endothelial growth factor (VEGF), might interact with the newer generation of antiangiogenic agents such as the monoclonal antibody bevacizumab (Avastin). 14,15Despite the rapidly expanding basic science research on the molecular targets affected by curcumin, extrapolation to clinical settings is problematic given the lack of large-scale trial evidence. Curcumin is incorporated with other natural compounds into adjunctive anticancer protocols on an anecdotal clinical basis, and preliminary data support synergistic combination of curcumin with genistein. 16-18

Although several potentially beneficial interactions with chemotherapeutic agents are listed later, these interactions have not been well studied, particularly in vivo. One research group has questioned the advisability of combining curcumin with alkylating agents such as cyclophosphamide, which induces apoptosis through activation of Janus kinase (JNK), which may be inhibited by relatively low doses of curcumin. 19 The same authors raised concerns about the advisability of coadministering curcumin with chemotherapy agents, which increase activation of NF-κB. Even though this may reduce drug-induced NF-κB–mediated drug resistance, the activation of NF-κB may be an important (but not exclusive) part of the cytotoxic mechanism of these drugs (e.g., doxorubicin), although this study has been criticized. 20 However, until further data are available with respect to specific chemotherapy agents and specific malignancies, decisions regarding coadministration of curcumin with chemotherapy need to be made in conjunction with practitioners experienced in the integrative oncological setting. There is also evidence, not detailed here, that curcumin may have beneficial interactions with radiotherapies. 21-23

Effects on Drug Metabolism and Bioavailability

Turmeric potentially exerts concerted effects on all three phases of drug metabolism. As with many herbs, the clinical implications of in vitro data remain to be established, and the interpretation of some studies is particularly controversial because of the extremely low bioavailability of curcumin. Biphasic effects have also been reported. In a Phase I study of 25 patients with various premalignant diagnoses, Cheng et al. 24 established that single oral doses of 8000 mg curcumin resulted in peak plasma concentrations of only 1.77. In colorectal adenocarcinoma patients who were administered curcumin for 7 days at 3600 mg/day, levels of curcumin were 2.5 times higher in malignant colorectal cells than in normal colon tissue, at 12.7 nmol/g in the form of sulfate and glucuronide conjugates. The effect of curcumin was to decrease levels of an oxidative deoxyribonucleic acid (DNA) adduct marker of cyclooxygenase-2 (COX-2) expression, which was not affected. 25,26In a rodent model, Shoba et al. 27 showed that coadministration of piperine (20 mg/kg) with curcumin increased the bioavailability of the herb by a factor of 154% in a single-dose pharmacokinetic study; in humans, 20 mg piperinen increased the bioavailability of curcumin by 2000%. 27 The low bioavailability results from rapid glucuronidation both hepatically and directly at the intestinal wall.

Effects on cytochrome P450 (CYP450) enzymes have been documented. Two different research groups used a rodent hepatocyte model to demonstrate curcumin inhibited both the induction and the activity of CYP450 1A1and 1A2, 2B1 and 2B2, and 2E1. 28-30The inhibitory effects were weak to moderate, except for 1A1/1A2, for which inhibition was more potent. These CYP450 enzymes are particularly related to metabolism of carcinogens, including the polycyclic aromatic hydrocarbons (PAHs). Using human oral mucosa cells and oral squamous cell carcinoma (SCC) cells, Rinaldi et al. 31 demonstrated induction of the nuclear translocation of the aryl hydrocarbon receptor (AhR), a process that leads to downstream activation of phase I and phase II AhR-responsive carcinogen-metabolizing enzymes. They also demonstrated increased CYP1A1 activity in oral SCC cells, combined with a decrease in carcinogen bioactivation, as well as an increase in intracellular reduced-glutathione (GSH) levels. The authors concluded that curcumin has a significant ability to modulate carcinogen activation in the human oral cavity. In a study by Raucy 32 using human hepatocytes, curcumin did not demonstrate any induction effects on CYP3A4, suggesting negligible interactions with the many drugs metabolized by this enzyme. Animal studies corroborate a significant effect of curcumin on phase II enzymes, particularly glutathione- S-transferase, and the ability of the curcuminoids to increase intracellular glutathione has been documented in several experimental models. 30,33,34

Several studies have demonstrated pronounced inhibitory effects of curcumin on P-glycoprotein (P-gp) in several cell lines, with dose-dependent effects at concentrations between 1 and 15 micromolar (μM). 35,36Anuchapreeda et al. 37 found that in human cervical carcinoma cells (KB-VI), pretreatment with curcumin at 1 to 10 μM for up to 72 hours significantly lowered MDR1 gene expression. Curcumin also inhibited rhodamine-123 efflux from these cells but had no effect on wild-type KB-3 cells that do not overexpress P-gp. The same research group later established that curcumin-I was the most effective inhibitory compound among the curcuminoids I to III, and that vinblastine sensitivity was increased in the homologous but drug-resistant KB-V1 line. 38 Nabekura et al. 36 established similar results for daunorubicin accumulation in the same drug-resistant cell line.

herb-drug interactions
Cisplatin and Related Platinum Chemotherapy Compounds
Cyclosporine and Related Immunosuppressive Agents
  • Evidence: Cyclosporine (Ciclosporin, cyclosporin A, CsA; Neoral, Sandimmune, SangCya).
  • Extrapolated, based on similar properties: Mycophenolate (CellCept).
Bimodal or Variable Interaction, with Professional Management
Impaired Drug Absorption and Bioavailability, Precautions Appropriate
Potential or Theoretical Beneficial or Supportive Interaction, with Professional Management

Probability: 4. Plausible
Evidence Base: Preliminary

Effect and Mechanism of Action

In a mixed pharmacodynamic and pharmacokinetic interaction, curcumin may enhance immunosuppressive activity of cyclosporine while reducing its bioavailability. The interaction has not been demonstrated clinically to date.


Chueh et al. 44 used a rodent cardiac allograft model to demonstrate that curcumin could effectively synergize with cyclosporine. Curcumin alone prolonged survival time of allograft rats compared with controls, but when combined with subtherapeutic doses of cyclosporine, the recipient animals survived longer than those with curcumin alone. Cytokine analysis suggested reduced levels of interleukin-2 (IL-2), interferon gamma (IFN-γ), and granzyme B in both the combination and the curcumin-only animals versus controls. Ranjan et al. 45 showed in vitro with human lymphocytes that curcumin inhibits T-cell activation through the CD28/B7 co-stimulation pathway. This pathway is resistant to cyclosporine suppression and synergistic suppression of T-cell responses. In a later study the same group showed curcumin suppressed NF-κB–mediated IL-2 release in response to mitogen activation by various stimuli. 46

Additional, if circumstantial, evidence for immunosuppressive effects comes from the ability of curcumin extracts to inhibit experimental allergic encephalomyelitis (a standard animal model of multiple sclerosis); this was mediated by interleukin-12–signaling blockade, resulting in decreased T-cell proliferation and T helper cell type 1 (Th1) differentiation. 47 A complication of any in vivo coadministration of cyclosporine with curcumin is that the drug is a substrate of P-gp, which is inhibited by curcumin, thus potentially decreasing bioavailability of cyclosporine. This was demonstrated, as an incidental finding, in an animal study examining the (lack of) effect of curcumin on cyclosporine-induced cholestasis and hypercholesterolemia. 48

Clinical Implications, Adaptations, and Integrative Therapeutics

Insufficient data are available to establish the clinical significance of this interaction. However, given the practice of measuring serum values for cyclosporine concentration during immunosuppressive therapy, the problems of adjusting to pharmacokinetic variation caused by P-gp inhibition are theoretically manageable. At present, the beneficial effect of the combination shown experimentally remains to be confirmed by clinical studies. Other evidence suggests a renal-protective effect of curcumin, renal toxicity being a known effect of cyclosporine.

Jones and Shoskes 49 showed that several plant-derived compounds reversed renal ischemia and reperfusion injury induced by mycophenolate (CellCept). Coadministration should be considered only with profession management, including monitoring of serum cyclosporine levels by the transplant providers.

Doxorubicin and Related Anthracycline Chemotherapy
Indomethacin, Related Nonsteroidal Anti-Inflammatory Drugs (NSAIDs), and Other Ulcerogenic Substances
Paclitaxel and Related Taxanes
Vinblastine, Related Vinca Alkaloids, and Platinum Chemotherapy Compounds
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Anticoagulants and Antiplatelet Drugs
Irinotecan/Camptothecin, Mechlorethamine
Oral Hypoglycemic Agents and Insulin
  • 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.WHO. Rhizoma curcumae longae. WHO Monographs on Selected Medicinal Plants. 1 vol. Geneva: World Health Organization; 1999:115-124.
  • 3.ESCOP. Curcumae longae rhizoma. ESCOP Monographs: the Scientific Foundation for Herbal Medicinal Products. 2nd ed. Exeter, UK: European Scientific Cooperative on Phytotherapy and Thieme; 2003:107-117.
  • 4.Aggarwal B, Kumar A, Aggarwal M, Shishodia S. Curcumin derived from turmeric (Curcuma longa): a spice for all seasons. In: Bagchi D, Preuss H, eds. Phytopharmaceuticals in Cancer Chemoprevention. Boca Raton, Fla: CRC Press; 2005:349-387.
  • 5.Frawley D, Lad V. The Yoga of Herbs. Twin Lakes, Wis: Lotus Press; 1986.
  • 6.Bensky D, Clavey S, Stogër E, Gamble A. Yu Jin. Chinese Herbal Medicine: Materia Medica. 3rd ed. Seattle: Eastland Press; 2004:609-612.
  • 7.Mills S, Bone K. The Essential Guide to Herbal Safety. St Louis: Churchill Livingstone; 2005.
  • 8.Chen J, Chen T. Chinese Medical Herbology and Pharmacology. City of Industry, Calif: Art of Medicine Press Inc; 2004.
  • 9.Chainani-Wu N. Safety and anti-inflammatory activity of curcumin: a component of tumeric (Curcuma longa). J Altern Complement Med 2003;9:161-168.View Abstract
  • 10.Kang G, Kong PJ, Yuh YJ et al. Curcumin suppresses lipopolysaccharide-induced cyclooxygenase-2 expression by inhibiting activator protein 1 and nuclear factor kappa B bindings in BV2 microglial cells. J Pharmacol Sci 2004;94:325-328.
  • 11.Yeh C-H, Chen T-P, Wu Y-C et al. Inhibition of NFκB activation with curcumin attenuates plasma inflammatory cytokines surge and cardiomyocytic apoptosis following cardiac ischemia/reperfusion. J Surg Res 2005;125:109-116.View Abstract
  • 12.Prusty BK, Das BC. Constitutive activation of transcription factor AP-1 in cervical cancer and suppression of human papillomavirus (HPV) transcription and AP-1 activity in HeLa cells by curcumin. Int J Cancer 2005;113:951-960.View Abstract
  • 13.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
  • 14.Yoysungnoen P, Wirachwong P, Bhattarakosol P et al. Effects of curcumin on tumor angiogenesis and biomarkers, COX-2 and VEGF, in hepatocellular carcinoma cell-implanted nude mice. Clin Hemorheol Microcirc 2006;34:109-115.View Abstract
  • 15.Hemaiswarya S, Doble M. Potential synergism of natural products in the treatment of cancer. Phytother Res 2006;20:239-249.View Abstract
  • 16.Verma SP, Goldin BR. Copper modulates activities of genistein, nitric oxide, and curcumin in breast tumor cells. Biochem Biophys Res Commun 2003;310:104-108.View Abstract
  • 17.Santibanez JF, Quintanilla M, Martinez J. Genistein and curcumin block TGF-beta 1-induced u-PA expression and migratory and invasive phenotype in mouse epidermal keratinocytes. Nutr Cancer 2000;37:49-54.View Abstract
  • 18.Verma SP, Salamone E, Goldin B. Curcumin and genistein, plant natural products, show synergistic inhibitory effects on the growth of human breast cancer MCF-7 cells induced by estrogenic pesticides. Biochem Biophys Res Commun 1997;233:692-696.
  • 19.Somasundaram S, Edmund NA, Moore DT et al. Dietary curcumin inhibits chemotherapy-induced apoptosis in models of human breast cancer. Cancer Res 2002;62:3868-3875.View Abstract
  • 20.Mitchell TM. Correspondence re: Somasundaram et al., Dietary curcumin inhibits chemotherapy-induced apoptosis in models of human breast cancer. Cancer Res 62:3868-3875, 2002. Cancer Res 2003;63:5165-5166; author reply 5166-5167.
  • 21.Khafif A, Hurst R, Kyker K et al. Curcumin: a new radio-sensitizer of squamous cell carcinoma cells. Otolaryngol Head Neck Surg 2005;132:317-321.View Abstract
  • 22.Khopde SM, Priyadarsini KI, Guha SN et al. Inhibition of radiation-induced lipid peroxidation by tetrahydrocurcumin: possible mechanisms by pulse radiolysis. Biosci Biotechnol Biochem 2000;64:503-509.View Abstract
  • 23.Van’t Land B, Blijlevens NM, Marteijn J et al. Role of curcumin and the inhibition of NF-κB in the onset of chemotherapy-induced mucosal barrier injury. Leukemia 2004;18:276-284.
  • 24.Cheng AL, Hsu CH, Lin JK et al. Phase I clinical trial of curcumin, a chemopreventive agent, in patients with high-risk or pre-malignant lesions. Anticancer Res 2001;21:2895-2900.View Abstract
  • 25.Garcea G, Berry DP, Jones DJ et al. Consumption of the putative chemopreventive agent curcumin by cancer patients: assessment of curcumin levels in the colorectum and their pharmacodynamic consequences. Cancer Epidemiol Biomarkers Prev 2005;14:120-125.View Abstract
  • 26.Sharma RA, McLelland HR, Hill KA et al. Pharmacodynamic and pharmacokinetic study of oral Curcuma extract in patients with colorectal cancer. Clin Cancer Res 2001;7:1894-1900.View Abstract
  • 27.Shoba G, Joy D, Joseph T et al. Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers. Planta Med 1998;64:353-356.View Abstract
  • 28.Thapliyal R, Maru GB. Inhibition of cytochrome P450 isozymes by curcumins in vitro and in vivo. Food Chem Toxicol 2001;39:541-547.View Abstract
  • 29.Thapliyal R, Deshpande SS, Maru GB. Effects of turmeric on the activities of benzo(a)pyrene-induced cytochrome P-450 isozymes. J Environ Pathol Toxicol Oncol 2001;20:59-63.View Abstract
  • 30.Oetari S, Sudibyo M, Commandeur JN et al. Effects of curcumin on cytochrome P450 and glutathione S-transferase activities in rat liver. Biochem Pharmacol 1996;51:39-45.View Abstract
  • 31.Rinaldi AL, Morse MA, Fields HW et al. Curcumin activates the aryl hydrocarbon receptor yet significantly inhibits (-)-benzo(a)pyrene-7R-trans-7,8-dihydrodiol bioactivation in oral squamous cell carcinoma cells and oral mucosa. Cancer Res 2002;62:5451-5456.
  • 32.Raucy JL. Regulation of CYP3A4 expression in human hepatocytes by pharmaceuticals and natural products. Drug Metab Dispos 2003;31:533-539.View Abstract
  • 33.Azuine MA, Bhide SV. Chemopreventive effect of turmeric against stomach and skin tumors induced by chemical carcinogens in Swiss mice. Nutr Cancer 1992;17:77-83.View Abstract
  • 34.Iqbal M, Sharma SD, Okazaki Y et al. Dietary supplementation of curcumin enhances antioxidant and phase II metabolizing enzymes in ddY male mice: possible role in protection against chemical carcinogenesis and toxicity. Pharmacol Toxicol 2003;92:33-38.View Abstract
  • 35.Zhou S, Lim LY, Chowbay B. Herbal Modulation of P-glycoprotein. Drug Metab Rev 2004;36:57-104.View Abstract
  • 36.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
  • 37.Anuchapreeda S, Leechanachai P, Smith MM et al. Modulation of P-glycoprotein expression and function by curcumin in multidrug-resistant human KB cells. Biochem Pharmacol 2002;64:573-582.View Abstract
  • 38.Chearwae W, Anuchapreeda S, Nandigama K et al. Biochemical mechanism of modulation of human P-glycoprotein (ABCB1) by curcumin I, II, and III purified from turmeric powder. Biochem Pharmacol 2004;68:2043-2052.
  • 39.Venkatesan N, Punithavathi V, Chandrakasan G. Curcumin protects bleomycin-induced lung injury in rats. Life Sci 1997;61:PL51-58.View Abstract
  • 40.Punithavathi D, Venkatesan N, Babu M. Curcumin inhibition of bleomycin-induced pulmonary fibrosis in rats. Br J Pharmacol 2000;131:169-172.View Abstract
  • 41.Navis I, Sriganth P, Premalatha B. Dietary curcumin with cisplatin administration modulates tumour marker indices in experimental fibrosarcoma. Pharmacol Res 1999;39:175-179.View Abstract
  • 42.Notarbartolo M, Poma P, Perri D et al. Antitumor effects of curcumin, alone or in combination with cisplatin or doxorubicin, on human hepatic cancer cells: analysis of their possible relationship to changes in NF-κB activation levels and in IAP gene expression. Cancer Lett 2005;224:53-65.View Abstract
  • 43.Venkatesan N, Chandrakasan G. Modulation of cyclophosphamide-induced early lung injury by curcumin, an anti-inflammatory antioxidant. Mol Cell Biochem 1995;142:79-87.View Abstract
  • 44.Chueh SC, Lai MK, Liu IS et al. Curcumin enhances the immunosuppressive activity of cyclosporine in rat cardiac allografts and in mixed lymphocyte reactions. Transplant Proc 2003;35:1603-1605.View Abstract
  • 45.Ranjan D, Johnston TD, Wu G et al. Curcumin blocks cyclosporine A–resistant CD28 costimulatory pathway of human T-cell proliferation. J Surg Res 1998;77:174-178.View Abstract
  • 46.Ranjan D, Chen C, Johnston TD et al. Curcumin inhibits mitogen-stimulated lymphocyte proliferation, NF kB activation, and IL-2 signaling. J Surg Res 2004;121:171-177.View Abstract
  • 47.Natarajan C, Bright JJ. Curcumin inhibits experimental allergic encephalomyelitis by blocking IL-12 signaling through Janus kinase–STAT pathway in T lymphocytes. J Immunol 2002;168:6506-6513.View Abstract
  • 48.Deters M, Klabunde T, Meyer H et al. Effects of curcumin on cyclosporine-induced cholestasis and hypercholesterolemia and on cyclosporine metabolism in the rat. Planta Med 2003;69:337-343.View Abstract
  • 49.Jones EA, Shoskes DA. The effect of mycophenolate mofetil and polyphenolic bioflavonoids on renal ischemia reperfusion injury and repair. J Urol 2000;163:999-1004.View Abstract
  • 50.Venkatesan N. Curcumin attenuation of acute Adriamycin myocardial toxicity in rats. Br J Pharmacol 1998;124:425-427.View Abstract
  • 51.Venkatesan N, Punithavathi D, Arumugam V. Curcumin prevents Adriamycin nephrotoxicity in rats. Br J Pharmacol 2000;129:231-234.View Abstract
  • 52.Chuang SE, Yeh PY, Lu YS et al. Basal levels and patterns of anticancer drug-induced activation of nuclear factor-kappaB (NF-κB), and its attenuation by tamoxifen, dexamethasone, and curcumin in carcinoma cells. Biochem Pharmacol 2002;63:1709-1716.View Abstract
  • 53.Harbottle A, Daly AK, Atherton K, Campbell FC. Role of glutathione S-transferase P1, P-glycoprotein and multidrug resistance–associated protein 1 in acquired doxorubicin resistance. Int J Cancer 2001;92:777-783.View Abstract
  • 54.Rukkumani R, Aruna K, Varma PS et al. Comparative effects of curcumin and an analog of curcumin on alcohol and PUFA induced oxidative stress. J Pharm Pharm Sci 2004;7:274-283.View Abstract
  • 55.Nanji AA, Jokelainen K, Tipoe GL et al. Curcumin prevents alcohol-induced liver disease in rats by inhibiting the expression of NF-kappa B–dependent genes. Am J Physiol Gastrointest Liver Physiol 2003;284:G321-327.View Abstract
  • 56.Rajakrishnan V, Jayadeep A, Arun OS et al. Changes in the prostaglandin levels in alcohol toxicity: effect of curcumin and N-acetylcysteine. J Nutr Biochem 2000;11:509-514.View Abstract
  • 57.Gukovsky I, Reyes CN, Vaquero EC et al. Curcumin ameliorates ethanol and nonethanol experimental pancreatitis. Am J Physiol Gastrointest Liver Physiol 2003;284:G85-G95.View Abstract
  • 58.Rajakrishnan V, Viswanathan P, Rajasekharan KN, Menon VP. Neuroprotective role of curcumin from Curcuma longa on ethanol-induced brain damage. Phytother Res 1999;13:571-574.View Abstract
  • 59.Rukkumani R, Aruna K, Varma PS, Menon VP. Curcumin influences hepatic expression patterns of matrix metalloproteinases in liver toxicity. Ital J Biochem 2004;53:61-66.View Abstract
  • 60.Naik RS, Mujumdar AM, Ghaskadbi S. Protection of liver cells from ethanol cytotoxicity by curcumin in liver slice culture in vitro. J Ethnopharmacol 2004;95:31-37.View Abstract
  • 61.Rajakrishnan V, Shiney SJ, Sudhakaran PR, Menon VP. Effect of curcumin on ethanol-induced stress on mononuclear cells. Phytother Res 2002;16:171-173.View Abstract
  • 62.Rafatullah S, Tariq M, Al-Yahya MA et al. Evaluation of turmeric (Curcuma longa) for gastric and duodenal antiulcer activity in rats. J Ethnopharmacol 1990;29:25-34.View Abstract
  • 63.Swarnakar S, Ganguly K, Kundu P et al. Curcumin regulates expression and activity of matrix metalloproteinases 9 and 2 during prevention and healing of indomethacin-induced gastric ulcer. J Biol Chem 2005;280:9409-9415.
  • 64.Kositchaiwat C, Kositchaiwat S, Havanondha J. Curcuma longa Linn. in the treatment of gastric ulcer comparison to liquid antacid: a controlled clinical trial. J Med Assoc Thai 1993;76:601-605.View Abstract
  • 65.Menon LG, Kuttan R, Kuttan G. Anti-metastatic activity of curcumin and catechin. Cancer Lett 1999;141:159-165.View Abstract
  • 66.Bava SV, Puliappadamba VT, Deepti A et al. Sensitization of Taxol-induced apoptosis by curcumin involves down-regulation of nuclear factor-kappaB and the serine/threonine kinase Akt and is independent of tubulin polymerization. J Biol Chem 2005;280:6301-6308.View Abstract
  • 67.Srivastava R, Puri V, Srimal RC, Dhawan BN. Effect of curcumin on platelet aggregation and vascular prostacyclin synthesis. Arzneimittelforschung 1986;36:715-717.View Abstract
  • 68.Srivastava R, Dikshit M, Srimal RC, Dhawan BN. Anti-thrombotic effect of curcumin. Thromb Res 1985;40:413-417.View Abstract
  • 69.Srivastava KC, Bordia A, Verma SK. Curcumin, a major component of food spice turmeric (Curcuma longa) inhibits aggregation and alters eicosanoid metabolism in human blood platelets. Prostaglandins Leukot Essent Fatty Acids 1995;52:223-227.View Abstract
  • 70.Shah BH, Nawaz Z, Pertani SA et al. Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor– and arachidonic acid–mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling. Biochem Pharmacol 1999;58:1167-1172.View Abstract
  • 71.Nishiyama T, Mae T, Kishida H et al. Curcuminoids and sesquiterpenoids in turmeric (Curcuma longa L.) suppress an increase in blood glucose level in type 2 diabetic KK-Ay mice. J Agric Food Chem 2005;53:959-963.View Abstract
  • 72.Kuroda M, Mimaki Y, Nishiyama T et al. Hypoglycemic effects of turmeric (Curcuma longa L. rhizomes) on genetically diabetic KK-Ay mice. Biol Pharm Bull 2005;28:937-939.View Abstract
  • 73.Suryanarayana P, Saraswat M, Mrudula T et al. Curcumin and turmeric delay streptozotocin-induced diabetic cataract in rats. Invest Ophthalmol Vis Sci 2005;46:2092-2099.View Abstract
  • 74.Arafa HM. Curcumin attenuates diet-induced hypercholesterolemia in rats. Med Sci Monit 2005;11:BR228-BR234.View Abstract
  • 75.Osawa T, Kato Y. Protective role of antioxidative food factors in oxidative stress caused by hyperglycemia. Ann N Y Acad Sci 2005;1043:440-451.View Abstract