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Although the great efficacy of isoniazid (INH) and rifampicin (RFP) combination in the treatment of tuberculosis,hepatotoxicity is the most pervasive serious complication.Taxifolin (TAX), belongs to a kind of flavonoids, has been proposed as a potent antioxidant.In this study, we aimed to investigate the molecular mechanism of the protective effects of TAX against INH-RFP induced injury in human L02 hepatocytes.Administration of INH-RFP combination (0.6 and 0.2 mM for 6 hours) resulted in hepatocyte apoptosis and a significant increase in the formation of reactive oxygen species (ROS) and lipid peroxidation products,decreasing glutathione content, superoxide dismutase and catalase activities, enhancing the expression of hepatic CYP3A4 and CYP2E1.Co-administration of TAX significantly ameliorated INH-RFP induced alteration.These effects were partly mediated through antiapoptosis, antioxidation, decrease in the combination-induced ROS and lipid peroxidation products.Furthermore, TAX attenuated INH-RFP induced the overexpression of CYP3A4 and CYP2E1.The collective evidence in this study indicated that TAX possessed the ability to protect hepatocytes against INH-RFP induced hepatotoxicity.