Abstract:To study the Jiangtangxiaoke granule in the treatment of high fat diet induced type 2 diabetes and to investigate its effect on renal N-terminal kinase signal pathway. Methods: All 72 Wistar rats were reared in SPF conditions, and were randomly divided into an intervention group, a control group and a normal control group, 24 rats in each. By streptozotocin (STZ) intraperitoneal injection of 30 mg/kg synergy, high fat diet induced type 2 diabetes animal models were built. After the model intervention, the normal control group received standard diet; the control group was treated with high glucose and high fat diet; the intervention group treated with high glucose, high fat diet, and Jiangtangxiaoke granules were calculated according to the body weight of 9 g/kg rats by gavage once daily. Treatment lasted 8 weeks. Using enzyme-linked immunosorbent assay (ELISA method) to detect rats blood glucose (Glu), triglyceride (TG), total cholesterol (TC), serum creatinine (Scr); routine HE staining, observing the changes of renal structure in each group; real time fluorescent polymerase chain reaction (q-PCR) detection (amino terminal kinase) and JNK (glucagon like peptide-1 GLP-1) and Western blotting (Western Blot) to detect the activation of JNK signaling pathway, JNK (phosphorylated N-terminal kinase) p-JNK and GLP-1.Results: 1) The Glu, TC, TG and Scr in the intervention group were significantly lower than those in the control group (P<0.05). 2) Compared with the control group, the changes of glomerular structure were significantly improved in the intervention group (P<0.05). 3) Compared with the normal control group, the expression of p-JNK protein in control group increased significantly (P<0.05), GLP-1 gene and protein significantly decreased (P<0.05); after treatment, the intervention group of p-JNK protein was lower than that of the control group (P<0.05), and GLP-1 (P<0.05) gene and protein increased. Conclusion: Jiangtangxiaoke granules can regulate sugar, lipid metabolism, protect the kidney function, its mechanism may be related to the inhibition of the JNK signaling pathway and regulation of GLP-1.