Objective：To investigate the clinical effect of Qinggan prescription on rats with fatty liver and its effect on oxidative damage factor and expression of Liver X Receptor(LXR)-α.Methods：Divided 60 SD rats into the normal group，the model group，the group of low-dose Qinggan prescription，the group of medium-dose Qinggan prescription，the group of high-dose Qinggan prescription，and the simvastatin group randomly，10 rats in each group.Except the normal group，all groups were given barley-based diets，2%of cholesterol，and 10%of lard to feed rats for six weeks.Fatty liver models of rat were duplicated.The simvastatin group was given 25.2 mg/(kg·d)of simvastatin by gavage.Qinggan prescription of low，middle and high dose groups were respectively given 5，10，and 15 g/(kg·d)of Qinggan prescription by gavage，while the normal group and the model group were given equivalent normal saline by gavage，once a day，lasting for six weeks.Compared blood lipid level and liver function in each group.Detected total antioxidant capacity(T-GSH)，superoxide dismutase activity(SOD)，level of malondialdehyde(MDA)，and expression of LXR- α mRNA in each group.Results：Compared with the normal group，total cholesterol(TC)，triglyceride(TG)，low density lipoprotein cholesterol(LDL-C)，free fatty acid(FFA)，alanine aminotransferase(ALT)，aspartate aminotransferase(AST)，LXR- α mRNA，and levels of MDA in the model group were all obviously increased， while high-density lipoprotein cholesterol(HDL-C)， SOD， and levels of T-GSH were all obviously decreased，differences being significant(P ＜ 0.01).Compared with the medium group，TC，TG，LDL-C，FFA，ALT，AST，LXR-α mRNA，and levels of MDA in the Qinggan prescription of low，medium and high dose groups and the simvastatin group were all evidently decreased，differences being significant(P＜ 0.05，P＜ 0.01).Conclusion：Qinggan prescription can significantly improve blood lipids and liver function in fatty liver model of rats，and improve hepatic lipid and liver function by promoting the ability of liver to remove lipid peroxidation products and to reduce the expression of LXR-α.