RESUMEN

The aim of this study was to evaluate the role of inflammation and oxidative damage in hepatotoxicity of ethanol. Also we assessed protective effects of atorvastatin against ethanol-induced hepatotoxicity. In this study, the animals were divided into five groups: control, ethanol (10 mg/kg intraperitoneal (i.p.)), ethanol with atorvastatin (10, 20 mg/kg/day, i.p.) and ethanol-vitamin C group which received ethanol (10 mg/kg/day) plus vitamin C (200 mg/kg, i.p.) for 28 consecutive days. Then, the animals were euthanized and liver tissues were separated. Biochemical markers ALT and AST were measured. Moreover, glutathione (GSH) content, lipid peroxidation, protein carbonyl, nitric oxide and tumor necrosis factor-α (TNF-α) were evaluated. The administration of ethanol for 28 days resulted in an increase in liver damage, oxidative stress and inflammatory markers. The atorvastatin was able to prevent the ethanol-induced hepatotoxicity by decreasing the oxidative stress and inflammation processes. Our study showed the critical role of oxidative damage and inflammation in ethanol-induced hepatotoxicity that markedly was inhibited by administration of atorvastatin. Therefore, atorvastatin can be suggested for prevention of ethanol-induced hepatotoxicity.