Ameliorative effect of curcumin on hepatotoxicity induced by chloroquine phosphate
Department of Zoology, University School of Sciences, Gujarat University, Ahmedabad 380009, Gujarat, India.Environmental toxicology and pharmacology 09/2010; 30(2):103-9. DOI: 10.1016/j.etap.2010.04.001
India is one of the most endemic areas, where malaria predominates and its control has become a formidable task. Chloroquine phosphate (CQ) on account of its rapid action on blood schizontocide of all the malarial parasite strains has become the most widely prescribed drug for prophylaxis and treatment of malaria. Toxicity of CQ is most commonly encountered at therapeutic and higher doses of treatment. Thus, the present study was undertaken to evaluate the protective effect of Curcumin, a herbal antioxidant obtained from Curcuma longa, on hepatic biochemical and histopathological status of CQ induced male mice. Swiss albino male mice were administered oral doses of CQ (100mg/kg body wt., 200mg/kg body wt. and 300mg/kg body wt.) and CQ+curcumin (300mg/kg body wt.+80mg/kg body wt.) for 45 days. A withdrawal of high dose treatment for 45 days was also studied. Administration of CQ brought about a significant decrease in Protein content with a decline in SDH, ATPase and ALKase activities, whereas ACPase activity was found to be significantly increased following CQ treatment. Antioxidant enzyme SOD registered a significant reduction as opposed to TBARS which was found to be elevated in a significant manner in the CQ treated groups as compared to control. Gravimetric indices (body weight and organ weight) declined significantly following CQ treatment. Administration of curcumin exhibited significant reversal of CQ induced toxicity in hepatic tissue. Protein content, SDH, ATPase, ALKase, ACPase, SOD, TBARS, body weight and organ weight were found to be comparable to that of control group after curcumin administration. Thus, obtained results led us to conclude the curative potential of curcumin against CQ induced hepatotoxicity.
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ABSTRACT: We have investigated the cardioprotective effects of exercise training and/or curcumin on lead acetate-induced myocardial damage. Forty rats were randomly divided into 5 groups: (1) lead acetate, (2) curcumin, (3) endurance training, (4) training + curcumin, (5) sham groups. The rats in groups 3 and 4 experienced the treadmill running of 15 to 22 m/min for 25 to 64 minutes, 5 times a week for 8 weeks. Groups 1 to 4 received lead acetate (20 mg/kg), the sham group received curcumin solvent (ethyl oleat), and the curcumin and training + curcumin groups received curcumin solution (30 mg/kg) intraperitoneally. Lead administration resulted in significant increases in high-sensitivity C-reactive protein (hs-CRP), creatine kinase-MB (CK-MB), malondialdehyde (MDA), and low-density lipoprotein (LDL), and significantly decreased glutathione peroxidase (GPx), Total Antioxidant Capacity (TAC), and high-density lipoprotein (HDL) levels. Treadmill running and\or curcumin supplementation resulted in a significant decrease in hs-CRP, CK-MB, MDA, and LDL levels and significantly increased GPx, TAC, and HDL levels. These results suggest a lifestyle-induced cardioprotective potential in ameliorating lead-induced cardiotoxicity.International Journal of Toxicology 03/2011; 30(2):190-6. DOI:10.1177/1091581810392809 · 1.29 Impact Factor
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ABSTRACT: Objective To evaluate the efficacy of curcumin in combating arsenic induced hepatic oxidative stress, histopathological changes and the hepatic arsenic accumulation in rat model.Methods Oxidative stress was induced by oral administration 4 mg/kg b.wt of arsenic trioxide (As2O3,) for 45 days in experimental rats. The level of liver arsenic concentration, lipid peroxidation, reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione-S-transferase (GST), and glutathione peroxidase (GPx) were determined in adult male Wistar rats. Hepatotoxicity was assessed by quantifying the aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phophatase (ALP). Hepatoprotective efficacy of curcumin (15 mg/kg b.wt) was evaluated by combination treatment with As2O3.ResultsAs2O3 administration leads to the generation of reactive oxygen species (ROS), arsenic accumulation, serum marker enzymes release and decrease in antioxidant enzymes in liver. Retention of arsenic in liver caused increased level of lipid peroxidation with a concomitant decline in the glutathione dependant antioxidant enzymes and antiperoxidative enzymes. Curcumin treatment protected the liver from arsenic induced deterioration of antioxidant levels as well as oxidative stress. And also a significant decrease in hepatic arsenic accumulation and serum marker enzymes was observed. Histopathological examination revealed a curative improvement in liver tissue.Conclusions These findings lead to the conclusion that curcumin may have the potential to protect the liver from arsenic-induced toxic effects.Asian Pacific Journal of Tropical Biomedicine 02/2012; 2(2):S706–S711. DOI:10.1016/S2221-1691(12)60300-1
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ABSTRACT: Rift Valley fever virus (RVFV) is an arbovirus that is classified as a select agent, an emerging infectious virus, and an agricultural pathogen. Understanding RVFV-host interactions is imperative to the design of novel therapeutics. Here, we report that an infection by the MP-12 strain of RVFV induces phosphorylation of the p65 component of the NFκB cascade. We demonstrate that phosphorylation of p65 (serine 536) involves phosphorylation of IκBα and occurs through the classical NFκB cascade. A unique, low molecular weight complex of the IKK-β subunit can be observed in MP-12-infected cells, which we have labeled IKK-β2. The IKK-β2 complex retains kinase activity and phosphorylates an IκBα substrate. Inhibition of the IKK complex using inhibitors impairs viral replication, thus alluding to the requirement of an active IKK complex to the viral life cycle. Curcumin strongly down-regulates levels of extracellular infectious virus. Our data demonstrated that curcumin binds to and inhibits kinase activity of the IKK-β2 complex in infected cells. Curcumin partially exerts its inhibitory influence on RVFV replication by interfering with IKK-β2-mediated phosphorylation of the viral protein NSs and by altering the cell cycle of treated cells. Curcumin also demonstrated efficacy against ZH501, the fully virulent version of RVFV. Curcumin treatment down-regulated viral replication in the liver of infected animals. Our data point to the possibility that RVFV infection may result in the generation of novel versions of host components (such as IKK-β2) that, by virtue of altered protein interaction and function, qualify as unique therapeutic targets.Journal of Biological Chemistry 07/2012; 287(40):33198-214. DOI:10.1074/jbc.M112.356535 · 4.57 Impact Factor
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