Effect of Bioflavonoid Quercetin on Endotoxin- Induced Hepatotoxicity and Oxidative Stress in Rat Liver
نویسندگان
چکیده
Septicaemia caused by gram-negative pathogens is a dangerous infection which is associated with high incidence of liver dysfunction. The severe and acute hepatotoxicity is presumably due to massive release of endotoxin into systemic circulation after bacterial killing. The direct toxic effect of endotoxin is probably due to the increased production of reactive oxygen intermediates as O2, peroxides and nitric oxide. Quercetin (QT) and its sugar conjugates are the most abundantly-distributed bioflavonoids in plant kingdom and has potent antioxidant properties. The present study is aimed at investigating effect of QT in salvaging endotoxin-induced hepatic dysfunction and oxidative stress in rat liver. Hepatotoxicity was induced by administrating lipopolysaccharide (LPS), in a single dose of 1 mg/kg intraperitoneally to the rats. Liver enzymes (alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST)), total bilirubin and total protein were measured in serum. Oxidative stress in liver tissue homogenates was estimated by measuring thiobarbituric acid reactive substances (TBARS), glutathione content (GSH) and superoxide dismutase (SOD). LPS induced a marked hepatic dysfunction evident by rise in serum levels of ALT, AST and decrease in total bilirubin (p<0.05). TBARS levels were significantly increased whereas GSH and SOD levels decreased in the liver homogenates of LPS-treated rats. Chronic treatment of QT successfully attenuated these effects of LPS. In conclusion, these findings suggest that QT attenuates LPS-induced hepatotoxicity possibly by preventing cytotoxic effects of NO, oxygen free radicals and cytokines.
منابع مشابه
Effect of Bioflavonoid Quercetin on Endotoxin-Induced Hepatotoxicity and Oxidative Stress in Rat Liver
Septicaemia caused by gram-negative pathogens is a dangerous infection which is associated with high incidence of liver dysfunction. The severe and acute hepatotoxicity is presumably due to massive release of endotoxin into systemic circulation after bacterial killing. The direct toxic effect of endotoxin is probably due to the increased production of reactive oxygen intermediates as O 2 - , p...
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