RESUMO
Aim To investigate the effect of salvianolic acid B ( SalB) on non-alcoholic fatty liver disease in high fat-induced ApoE knockout mice by regulating AMPK-induced autophagy. Methods Healthy, 8 weeks old, homologous C57BL/6J mice and ApoE_/" mice were randomly divided into control group, model group and Sal B group, fed with high fat diet, intraperitoneal injection of Sal B ( 15 mg • kg"1 • d "') in group Sal B on week 8, and control group and model group were given an equal dose of normal saline. Pathological changes of livers in each group were assessed by HE staining, oil red 0 staining and Masson staining. Biochemical indexes in serum were analyzed commercially available kits. The levels of inflammation and oxidative stress in liver were detected by immuno-histochemistry. Autophagy and AMPK levels were determined by Western blot immunofluorescence. Results In model group, AST and ALT were significantly elevated in serum, and a large number of fat vacuoles and severe lipid deposits and collagen fibrosis were de-tected in liver. The liver lesions were significantly improved after SalB intervention compared with the ApoE~/_group. The levels of hepatic inflammation and oxidative stress significantly increased in model group but significantly decreased in SalB group. The levels of autophagy and AMPK were significantly, reduced in model group and markedly elevated in SalB group. Conclusions Sal B can improve non-alcoholic fatty liver disease in ApoE_/" mice, and the mechanism may involve mediating AMPK level and enhancing autophagy levels in liver.