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Objective: The aims were to investigate the effect of glucagon-like peptide-1 (GLP-1) on diet induce non-alcoholic fatty liver disease (NAFLD) and JNK signaling in rats.Methods: 30 male rats were randomly divided into three groups in which they were fed with normal diet (ND), high-fat diet (HFD), high-fat diet with liraglutide (GLP-1, first 12 weeks with HFD, later 4 weeks with liraglutide) for 16 weeks respectively.After feeding, the rats were sacrificed, their blood samples and liver tissues were collected.Levels of aminotransferase (ALT), aspartate-aminotransferase (AST), fasting blood glucose (FBG), triglyceride (TG) and total-cholesterol (TC) were detected by biochemistry automatic analyzer.Expression levels of free fatty acid (FFAs), superoxide dismutase (SOD) and malondial-dehyde (MAD) were by RIA.Tumor necrosis factor-a (TNF-a), adiponectin (ADP) and fasting insulin (FINS) expression level were by ELISA.JNK-1 and P-JNK1 were by Western blot.Results: Compared with the ND group, body weight, liver index, HOMA-IR, serum and liver homogenates levels of TG, TC, ALT, FBG and TC, TC, MAD, FFAs, TNF-a, ADP and expression of JNK1 and p-JNK1 in the HFD group were significantly increased, whereas level of SOD decreased significantly (P<0.05).The above markers were all markedly resumed in the GLP-1 group than those in the HFD group (P<0.05).Conclusion: Liraglutide has an anti-inflammatory effect on NAFLD rats, which is conducted by decreasing liver tissue inflammation index level, improving insulin resistance and liver pathological indexes, and the mechanism may be associated with increasing level of adiponectin and reducing excessive expression of JNK1 and p-JNK1.