Effect of Erchen Decoction on Rat Model with Type 2 Diabetes Mellitus and Nonalcoholic Fatty Liver Based on the SIRT1/UCP2 Signaling Pathway

OBJECTIVE To explore the effects and potential mechanisms of Erchen decoction on the glycolipid metabolism and oxidative stress in type 2 diabetes mellitus(T2DM) rats with nonalcoholic fatty liver desease(NAFLD). METHODS Forty ♂ SD rats were randomly selected as the normal control group, and 10 rats were randomly selected as the normal control group. After the other rats were successfully modeled, 20 rats were randomly selected and divided into the model group and the Erchen decoction group with 10 rats in each group. The rats were fed with basic diet in normal control group. The rats in model group were given high-fat and high-sugar diet and given intraperitoneal injection of streptozotocin 30 mg·kg^-1 once to prepare the T2DM combined with NAFLD model. The rats in Erchen decoction group were given Erchen decoction (1.0 g·mL^-1 dried herbs per day). After 12 weeks, biochemical and oxidative stress indicators of rats were measured. HE staining was employed to evaluate the pathological changes of liver in rats. Immunohistochemistry, q-PCR, and Western blotting were used to measure the expression of SIRT1/UCP2 pathway in the liver tissues. RESULTS Compared with the model group, Erchen decoction ameliorated observably the body weight and the metabolic function of rats, and decreased the levels of FBG, ALT, AST, TG, TC, LDL-C, VLDL, FFA, FINS, HOMA-IR and MDA, HDL, SOD, GSH-Px and CAT were significantly increased. The HE staining results showed that hepatic tissues in the model group had severe steatosis. Erchen decoction alleviated hepatocyte steatosis. The immunochemistry, q-PCR, and Western blotting results showed that compared with the model group, the mRNA and protein expression of SIRT1 were significantly increased, as well as the mRNA and protein expression of UCP2 were significantly reduced in the Erchen decoction group. CONCLUSION Erchen decoction can improve the T2DM rats with NAFLD to some extent, the mechanism of which may be associated with the regulating of SIRT1/UCP2 pathway.