丹蛭降糖胶囊联合运动对糖尿病大鼠胰腺JNK信号通路的影响

目的：观察丹蛭降糖胶囊联合运动对糖尿病大鼠胰腺c—Jun氨基末端激酶（c—Jun N-terminal kinase，JNK）信号通路的影响，探讨其治疗糖尿病的可能机制。方法：雄性Wistar大鼠78只，用小剂量链脲佐菌素联合高脂饲料的方法建立糖尿病大鼠模型，并将造模成功的60只大鼠分为模型组、运动组、丹蛭降糖胶囊组及运动联合丹蛭降糖胶囊组；另取12只大鼠作为正常对照。治疗8周后，用免疫组织化学法、蛋白质印迹法检测大鼠胰腺组织中磷酸化JNK（phospho-JNK，p-JNK）、胰腺十二指肠同源异型盒基因1（pancreatic and duodenal homeobox-1，PDX-1）及胰岛素的表达水平。结果：模型组胰腺组织中的P—JNK表达水平明显高于正常对照组（P〈0．01），而PDX-1和胰岛素含量则明显低于正常对照组（P〈0．01）；给予中药、运动干预能明显抑制JNK的活性，提高PDX-1和胰岛素的表达水平（P〈0．05，P〈0．01）。结论：运动及丹蛭降糖胶囊联用可能是通过抑制糖尿病大鼠JNK信号通路，对糖尿病胰岛β细胞起保护作用。

Effects of Chinese herbal medicine Danzhi Jiangtang Capsule and exercise on JNK signaling pathway in pancreatic tissues of diabetic rats

OBJECTIVE ： To explore the effects of exercise and Danzhi Jiangtang Capsule （DJC）, a compound traditional herbal medicine, on the JNK signaling pathway in pancreatic tissues of diabetic rats and to investigate the possible mechanisms of exercise and DJC in treating diabetes. METHODS= Seventy-eight male Wistar rats were injected with low dose of streptozotocin and fed a high-fat diet to establish a diabetic model in rats. Then 60 diabetic rats were divided into diabetes group, exercise group, DJC group and exercise combined with DJC group. Another twelve rats were used as normal control. After eight months of treatment, the expression levels of phosphor-c-Jun N-terminal kinase （p-JNK）, pancreatic and duodenal homeobox-1 （PDX-1）, and insulin protein in pancreatic tissues from rats were detected by immuno- histochemical method and Western blotting. RESULTS： In pancreatic tissues of diabetes group, the expression level of p-JNK protein was significantly higher than that in the normal group （P〈0.01）, and the expression levels of PDX-1 and insulin protein were significantly decreased （P〈0.0]）. After administration of exercise and DJC, the expression level of p-JNK protein in pancreatic tissues of the diabetes group was decreased significantly, while the expression levels of PDX-1 and insulin protein were increased significantly （P〈0.05 or P〈0.01）. CONCLUSION= Exercise and DJC effectively protect islet β-cell function in diabetic rats, which might be due to a decreased JNK signaling pathway.