Abstract
Iron overload is one of mechanisms by which hepatitis C virus causes oxidative stress that may contribute to fibrosis and carcinogenesis in the liver. Chronic hepatitis C (CHC) virus infection is a leading cause of progressive liver fibrosis, liver cirrhosis and hepatocellular carcinoma. Liver fibrosis with high mortality rate after diagnosis and limited successful treatment. The present study was designed to screen the potential hepatoprotective dose of deferiprone (DFP) and whether it can attenuate hepatotoxicity induced by concanavalin A (con A) in rats. Male Wister rats were randomized into 6 groups and treated with Con A (20 mg/kg, once, i.v) and/ordeferiprone (5, 10, 25 or 40 mg/kg/day, one hour before con A). Liver enzymes levels were assessed in addition to histopathological examination of liver tissues. DFP (5 mg/kg) pre-treatment restored liver enzymes toward normal values. Moreover, histopathological examination confirmed the protective effect of this dose of DFP.
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