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PubMed2002

Curcumin suppresses activation of NF-kappaB and AP-1 induced by phorbol ester in cultured human promyelocytic leukemia cells.

Many components that are derived from medicinal or dietary plants possess potential chemopreventive properties. Curcumin, a yellow coloring agent from turmeric (Curcuma longa Linn, Zingiberaceae), possesses strong antimutagenic and anticarcinogenic activities. In this study, we have found that curcumin inhibits the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced nuclear factor kB (NF-kappaB) activation by preventing the degradation of the inhibitory protein IkBalpa; and the subsequent translocation of the p65 subunit in cultured human promyelocytic leukemia (HL-60) cells. Alternatively, curcumin repressed the TPA-induced activation of NF-kappaB through direct interruption of the binding of NF-kappaB to its consensus DNA sequences. Likewise, the TPA-induced DNA binding of the activator protein-1 (AP-1) was inhibited by curcumin pretreatment.

Anticarcinogenic Agents↗

PubMedDate not supplied

The inhibitory effect of curcumin, genistein, quercetin and cisplatin on the growth of oral cancer cells in vitro.

Epidemiological evidence indicates that plant derived flavonoids and other phenolic antioxidants protect against heart disease and cancer. In the current investigation utilizing human oral squamous carcinoma cell line (SCC-25), we have evaluated the potency of three different plant phenolics, viz., curcumin, genistein and quercetin in comparison with that of cisplatin on growth and proliferation of SCC-25. Test agents were dissolved in DMSO and incubated in triplicates in 25 cm2 flasks in DMEM- HAM's F-12 (50:50)supplemented with 10% calf serum and antibiotics in an atmosphere 5% CO2 in air for 72 hours cell growth was determined by counting the number of cells in a hemocytometer. Cell proliferation was determined by measuring DNA synthesis by the incorporation of [3H]-thymidine in nuclear DNA. Cisplatin (0.1, 1.0, 10.0 microM) and curcumin (0.1, 1.0, 10.0 microM) induced significant dose-dependent inhibition in both cell growth as well as cell proliferation. Genistein and quercetin (1.0, 10.0, 100.0 microM) had biphasic effect, depending on their concentrations, on cell growth as well as cell proliferation. Based on these findings, it is concluded that curcumin is considerably more potent than genistein and quercetin, but cisplatin is five fold more potent than curcumin in inhibition of growth and DNA synthesis in SCC-25.

Antineoplastic Agents↗

PubMedDate not supplied

Chemopreventive effects of curcumin on glandular stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine and sodium chloride in rats.

The modifying effects of pure curcumin on glandular stomach carcinogenesis were investigated during the post-initiation phase in male Wistar rats treated with N-methyl-N'-nitro-N-nitrosoguanisine (MNNG) and sodium chloride. A total of 110 male 6-week-old rats were divided into four groups. Groups 1-3 (consisting of 30 rats/group) were given MNNG in their drinking water at a concentration of 100 ppm and simultaneously fed a diet supplemented with 5% NaCl for 8 weeks. They were then fed a diet containing either 0.2% (group 1) or 0.05% (group 2) pure curcumin or kept on a basal diet alone (group 3) for 55 weeks. The rats of the curcumin-treated groups (groups 1 and 2) were then switched to the basal diet for the following 4 weeks before sacrifice. Group 4 (20 rats) served as a non-treatment control. The total incidence of combined atypical hyperplasias and adenocarcinomas in the glandular stomachs was rather lower in groups 1 (93%) and 2 (90%) than in group 3 (100%), albeit without statistical significance. However, the mean number of atypical hyperplasias or adenocarcinomas of the glandular stomachs in group 1 (4.70) was significantly less than the value of group 3 (7.17) (p<0.05). Thus, the development of cancerous and precancerous lesions in the glandular stomach was decreased by exposure to pure curcumin. The present results indicate that the compound exerts chemopreventive effects, when given during the post-initiation phase of glandular stomach carcinogenesis in rats.

Adenocarcinoma↗

PubMed2002

Biodegradable microspheres of curcumin for treatment of inflammation.

Curcumin, a natural constituent of Curcuma longa (turmeric, CAS 458-37-7) was formulated as prolonged release biodegradable microspheres for treatment of inflammation. Natural biodegradable polymers, namely, bovine serum albumin and chitosan were used to encapsulate curcumin to form a depot forming drug delivery system. Microspheres were prepared by emulsion-solvent evaporation method coupled with chemical cross-linking of the natural polymers. Curcumin could be encapsulated into the biodegradable carriers upto an extent of 79.49 and 39.66% respectively with albumin and chitosan. Different drug:polymer ratios did not affect the mean particle size or particle size distribution significantly. However, the concentration of the crosslinking agent had remarkable influence on the drug release. In-vitro release studies indicated a biphasic drug release pattern, characterized by a typical burst-effect followed by a slow release which continued for several days. Evaluation of antinflammatory activity using Freund's adjuvant induced arthritic model in Wistar rats revealed significant difference between both the formulations, albumin microspheres and chitosan micropheres as well as against control. It was evident from the present study that the curcumin biodegradable microspheres could be successfully employed as prolonged release drug delivery system for better therapeutic management of inflammation as compared to oral or subcutaneous route.

Absorbable Implants↗

PubMed1992

Inhibition of lipid peroxidation and cholesterol levels in mice by curcumin.

Effect of oral administration of curcumin (diferuloyl methane) on lipid peroxidation in various organs of mice like liver, lung, kidney and brain was studied in control animals as well as those given carbon tetrachloride, paraquat and cyclophosphamide. Oral administration of curcumin significantly lowered the increased peroxidation of lipids in these tissues produced by these chemicals. Administration of curcumin was also found to lower significantly the serum and tissue cholesterol levels in these animals, indicating that the use of curcumin helps in conditions associated with peroxide induced injury such as liver damage and arterial diseases.

Animals↗

PubMed1992

Effect of oral curcumin administration on serum peroxides and cholesterol levels in human volunteers.

The effect of curcumin administration in reducing the serum levels of cholesterol and lipid peroxides was studied in ten healthy human volunteers, receiving 500 mg of curcumin per day for 7 days. A significant decrease in the level of serum lipid peroxides (33%), increase in HDL Cholesterol (29%), and a decrease in total serum cholesterol (11.63%) were noted. As curcumin reduced serum lipid peroxides and serum cholesterol, the study of curcumin as a chemopreventive substance against arterial diseases is suggested.

Administration, Oral↗

PubMed2003

[Protective effect of curcumin on experimental liver injury in mice].

OBJECTIVE: To Study the protective effect of curcumin on three models of experimental liver injury in mice. METHOD: The experimental models of live injury were induced by carbon tetrachloride (CCl4), D-galactosamine (D-Gal N), and Bacillus Calmette-Guerin (BCG) Plus lipolysaccharides (LPS), respectively, in mice. The serum ALT, AST, NO and liver MDA were measured to evaluate the protective effect of curcumin on experimental injury in mice. RESULT: Curcumin (50 mg.kg-1, 100 mg.kg-1, 150 mg.kg-1), like biophenyldicarboxylate, were shown to significantly inhibit the increase of serum ALT, AST, NO and liver molondialdehyde (MDA) content induced by CCl4, D-Gal N, BCG + LPS. CONCLUSION: Curcumin showed protective effect against liver injury induced by CCl4, D-Gal N, BCG plus LPS.

Alanine Transaminase↗

PubMed2004

Antioxidant effect of curcumin in selenium induced cataract of Wistar rats.

Wistar rat pups treated with curcumin, a natural constituent of Curcuma longa before being administered with selenium showed no opacities in the lens. The lipid peroxidation, xanthine oxidase enzyme levels in the lenses of curcumin and selenium co-treated animals were significantly less when compared to selenium treated animals. The superoxidase dismutase and catalase enzyme activities of curcumin and selenium co-treated animal lenses showed an enhancement. Curcumin co-treatment seems to prevent oxidative damage and found to delay the development of cataract.

Animals↗

PubMedDate not supplied

Modulatory effects of curcumin on lipid peroxidation and antioxidant status during nicotine-induced toxicity.

Nicotine, a pharmacologically active substance in tobacco, has been identified as a major risk factor for lung diseases. In the present study, we evaluated the protective effects of curcumin on tissue lipid peroxidation and antioxidants in nicotine-treated Wistar rats. Lung toxicity was induced by subcutaneous injection of nicotine at a dose of 2.5 mg/kg (5 days a week, for 22 weeks). Curcumin (80 mg/kg) was given simultaneously by intragastric intubation for 22 weeks. The enhanced level of tissue lipid peroxides in nicotine-treated rats was accompanied by a significant decrease in the levels of ascorbic acid, vitamin E, reduced glutathione, glutathione peroxidase, superoxide dismutase and catalase. Administration of curcumin significantly lowered the level of lipid peroxidation and enhanced the antioxidant status. The results of the present study suggest that curcumin exerts its protective effect against nicotine-induced lung toxicity by modulating the extent of lipid peroxidation and augmenting antioxidant defense system.

Animals↗

PubMed2004

Peroxynitrite interaction with curcumin solubilized in ethanolic solution.

Spectroscopic (fluorescence and absorptiometric) techniques were used to study the interaction between peroxynitrite, a known biological stressor, and curcumin, a potent biological antioxidant. In both techniques, the observed signals increased asymptotically until the concentration of peroxynitrite equals that of the curcumin, which was held constant at 1 x 10(-5) M. However, there was a shift in fluorescence wavelength after initial apparent oxidation of the hydroxyl group. This is perhaps due to nitration of the phenoxyl group of curcumin. The obtained data, using these techniques, suggest a second order reaction rate for the nitration of the curcumin by peroxynitrite. The biomolecular interaction or association constant obtained was 1.2 x 10(6)/M-s using the fluorescence technique and it was 3.6 x 10(6)/M-s using the absorptiometric technique. These values are in good agreement with literature values.

Antioxidants↗

PubMed2004

Curcumin influences hepatic expression patterns of matrix metalloproteinases in liver toxicity.

Hepatic fibrosis is a result of an imbalance between enhanced matrix synthesis and diminished breakdown of connective tissue proteins, the net result of which is increased deposition of Extra Cellular Matrix. In this concept Matrix Metalloproteinases play an important role because their activity is largely responsible for extra cellular matrix breakdown. In the present study we have tested the influence of curcumin, the active principle of turmeric, on matrix metalloproteinase expression during alcohol and thermally oxidised sunflower oil induced liver toxicity. Male albino Wistar rats were used for the study. The matrix metalloproteinase expressions were found to be increased significantly in alcohol as well as thermally oxidised sunflower oil groups and on treatment with curcumin there was a significant decrease. In alcohol + thermally oxidised sunflower oil group, we found a significant decrease in matrix metalloproteinase activities. Administration of curcumin significantly improved their activities. From the results obtained, we could conclude that curcumin influences the hepatic matrix metalloproteinases and effectively protects liver against alcohol and delta PUFA induced toxicity.

Animals↗

PubMed2004

[Study on preparation of the inclusion compound of curcumin with beta-cyclodextrin].

OBJECTIVE: The inclusion compound of curcumin with, beta-CD was preparated to increase the solubility and bioavaliability of curcumin. METHODS: Prepare inclusion compound was studied with orthogonal design. The inclusion compound was verified with fluorometry, TLC, and phase solubility. RESULT: The best way to prepare inclusion compound are as follows: the molar ratio between curcumin and, beta-CD is 1:1, temperture is 40 degrees C, reaction time is 2 h. CONCLUSION: Solubility of inclusion compound is 10 times than curcumin.

Biological Availability↗

PubMed2005

[Effect of curcumin on expression of human low density lipoprotein receptors in Xenopus Laevis oocytes].

OBJECTIVE: To investigate the molecular mechanism of curcumin in reducing blood lipids by establishing gene expression system of human low density lipoprotein receptors (LDL-R) in Xenopus Laevis oocytes (XLO). METHODS: The expression of LDL-R on cytomembrane was determined using immuno-fluorescent, ligand-fluorescent and immune colloidal gold techniques after human LDL-R containing p3.7 LDL plasmid was led into nucleus. And the expression of LDL-R gene in XLO was quantitatively determined by ELISA after being interfered with different concentrations of curcumin. RESULTS: The human LDL-R gene could be expressed on XLO, which could be significantly enhanced by curcumin in a dose-dependent manner. Conclusion One of the paths of curcumin in reducing blood lipids and anti-atherosclerosis was improving LDL-R gene expression and increasing the LDL-cholesterol absorption of cells.

Animals↗

PubMed2005

[Protective effect of curcumin on myocardial ischemia reperfusion injury in rats].

OBJECTIVE: To study the protective effect of curcumin on myocardial reperfusion injury in rats. METHODS: Myocardial ischemia reperfusion injury model was established by occluding the left anterior descending branch of coronary arter for 60 min and removing the ligation later to reperfuse for 60 min in vivo. Different dose of curcumin were administered by intravenous injection 5 min before the onset of ischemia. The changes of myocardial infarct sizes (MIS), the serum creatine phosphokinase (CK) and lactate dehydrogenase (LDH), the myocardial malondialdehyed (MDA) and free fatty acid (FFA) content, the myocardial super oxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity were measured. RESULTS: Curcumin (20, 40 mg/kg) reduced the myocardial infarct sizes, the serum CK and LDH activity. The myocardial MDA and FFA content all declined. SOD and GSH-Px activity were increased markedly. CONCLUSION: Curcumin exerts protective effects on myocardial ischemia reperfusion injury, which may be due to its function of inhibition of lipid peroxidation, augmentation of endogenous antioxidants and improving myocardial metabolism.

Animals↗

PubMed2006

Curcumin inhibits hypoxia-induced angiogenesis via down-regulation of HIF-1.

Hypoxia-inducible factor-1 (HIF-1) has a central role in cellular responses to hypoxia, including the transcriptional activation of a number of genes involved in angiogenesis in tumors. We found that curcumin, a natural, biologically active compound isolated from the commonly used spice turmeric, significantly decreases hypoxia-induced HIF-1alpha protein levels in HepG2 hepatocellular carcinoma cells. Moreover, curcumin suppressed the transcriptional activity of HIF-1 under hypoxia, leading to a decrease in the expression of vascular endothelial growth factor (VEGF), a major HIF-1 target angiogenic factor. Curcumin also blocked hypoxia-stimulated angiogenesis in vitro and down-regulated HIF-1alpha and VEGF expression in vascular endothelial cells. These findings suggest that curcumin may play pivotal roles in tumor suppression via the inhibition of HIF-1alpha-mediated angiogenesis.

Cell Growth Processes↗

PubMed2006

Curcumin induces cell death without oligonucleosomal DNA fragmentation in quiescent and proliferating human CD8+ cells.

UNLABELLED: Cytotoxic CD8+ cells play an important role in determining host response to tumor, thus chemotherapy is potentially dangerous as it may lead to T cells depletion. The purpose of this study was to elucidate the propensity of quiescent and proliferating human CD8+ cells to undergo cell death upon treatment with curcumin, a natural dye in Phase I of clinical trials as a prospective chemopreventive agent. METHODS: We treated human quiescent or proliferating CD8+ cells with 50 microM curcumin or irradiated them with UVC. Cell death symptoms such as decreased cell viability, chromatin condensation, activation of caspase-3 and specific DFF40/CAD endonuclease and oligonucleosomal DNA fragmentation were analyzed using MTT test, microscopic observation, Western blotting and flow cytometry. RESULTS: Curcumin decreased cell viability, activated caspase-3 and decreased the level of DFF45/ICAD, the inhibitor of the DFF40/CAD endonuclease. However, this did not lead to oligonucleosomal DNA degradation. In contrast, UVC-irradiated proliferating, but not quiescent CD8+ cells revealed molecular and morphological changes characteristic for apoptosis, including oligonucleosomal DNA fragmentation. Curcumin can induce cell death in normal human lymphocytes both quiescent and proliferating, without oligonucleosomal DNA degradation which is considered as a main hallmark of apoptotic cell death. Taking into account the role of CD8+ cells in tumor response, their depletion during chemotherapy could be particularly undesirable.

Antineoplastic Agents↗

PubMed1990

Sister chromatid exchange and chromosome aberrations induced by curcumin and tartrazine on mammalian cells in vivo.

Sister chromatid exchanges (SCEs) and chromosomal aberrations induced by curcumin (a natural dye) and tartrazine (a synthetic dye) were studied on bone marrow cells of mice and rats following acute and chronic exposure via the diet. Except for two low concentrations in the curcumin and one low concentration in the tartrazine treated series a significant increase in SCEs was observed in all the concentrations of the two dyes tested. Except for two high concentrations during the 9 months treatment no significant increase in chromosomal aberrations was observed in the curcumin treated series, whereas tartrazine showed a significant increase in chromosomal aberrations in some of the higher concentrations in all the series tested. The results indicate that tartrazine is more clastogenic than curcumin.

Animals↗

PubMed1986

Effect of curcumin on platelet aggregation and vascular prostacyclin synthesis.

In vitro and ex vivo effects of 1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione (diferuloylmethane, curcumin) and acetylsalicylic acid (ASA) on the synthesis of prostacyclin (PGI2) and on platelet aggregation has been studied in rat. Both drugs inhibited adenosine diphosphate (ADP)-, epinephrine (adrenaline)- and collagen-induced platelet aggregation in monkey plasma. Pretreatment with ASA (25-100 mg/kg), but not curcumin (100-300 mg/kg), inhibited PGI2 synthesis in rat aorta. In the in vitro system, too, curcumin caused a slight increase in the synthesis of PGI2, while ASA inhibited it. Curcumin may, therefore, be preferable in patients prone to vascular thrombosis and requiring antiarthritic therapy.

Adenosine Diphosphate↗