HMG-CoA reductase inhibitor, rosuvastatin averted carbon tetrachloride-induced oxidative stress, inflammation and fibrosis in the liver of rats

The aim of this study was to examine the effect of rosuvastatin in experimentally-induced hepatic inflammation and fibrosis in rats. Carbon tetra chloride (CCl4) was administered orally to induce liver damage in female Long Evans rats. Rats were treated with CCl4 alone twice a week over two weeks. Rosuvastatin (10 mg/kg) was also given daily to CCl4 treated rats concurrently by nasogastric gavage. After two weeks, various oxidative stress markers as well as liver markers enzymes were investigated in different animal groups tested in this study. Moreover, histological assessments were also done for inflammatory cell infiltration and fibrosis in the liver of all test groups. Plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities were increased in the CCl4 group compared with the control group. Increased liver enzyme activities were significantly decreased by rosuvastatin treatment. Moreover, rosuvastatin treatment inhibited the formation of lipid peroxidation products in CCl4 administered rats. Rosuvastatin treatment also restored the decreased superoxide dismutase (SOD) activities as well as elevated the reduced glutathione concentration in CCl4 administered rats. Liver tissues from rats of control group also revealed no significant pathological changes, while CCl4 administered rats showed significant infiltration of inflammatory cells and liver fibrosis, which was further, normalized or significantly decreased by rosuvastatin treatment. This study revealed that, rosuvastatin treatment may ameliorate all necro-inflammatory and fibrotic changes in liver tissues of CCl4 induced rats and could be used as an alternative therapy for chemical or drug-induced liver fibrosis.