【摘要】 目的研究替普瑞酮(TEPN)对2型糖尿病的降血糖作用及其机制。方法给予2型糖尿病模型大鼠口服TEPN(75、150 mg/kg)和二甲双胍(45 mg/kg)4周,观察动物空腹血糖、胰岛素、胆固醇、甘油三酯、游离脂肪酸、热休克蛋白(HSP)70以及肝脏、胰腺、脂肪和肌肉组织HSP70与肝脏JNK、p-JNK的表达水平。结果与模型对照组比较,TEPN给药组和二甲双胍组动物的空腹血糖、胰岛素、胆固醇、甘油三酯、游离脂肪酸明显更低,血清HSP70水平明显更高(P<0.05)。与模型对照组比较,TEPN给药组动物的肝脏、胰腺和肌肉组织中HSP70的表达水平明显更高,肝脏组织中JNK和p-JNK的表达水平明显更低(P<0.05)。结论 TEPN对2型糖尿病大鼠模型有降血糖作用,其机制可能与提高血清和组织HSP70水平、抑制JNK信号转导通路有关。更多还原

【Abstract】 Objective To study the hypoglycemic effect and mechanism of teprenone(TEPN) on type 2 diabetes mellitus in rat. Methods The type 2 diabetes mellitus model rats were given TEPN(75, 150 mg/kg) and metformin(45 mg/kg)orally for 4 weeks. The levels of fasting glucose, insulin cholesterol, triglycerides, free fatty acid, heat shock protein(HSP)70 as well as the expression levels of HSP70 in liver, pancreas, fat and muscle and the expression levels of JNK and p-JNK in liver were observed. Results Compared with the model control group, the levels of fasting glucose, insulin,cholesterol, triglycerides, free fatty acid significantly reduced and serum HSP70 increased in the TEPN group and metformin group(P<0.05). Compared with the model control group, the expression levels of HSP70 in the liver, pancreas and muscle significantly improved, and the expression levels of JNK and p-JNK in the liver significantly reduced in the TEPN group(P<0.05). Conclusion TEPN have hypoglycemic effect on type 2 diabetic mellitus rats, its mechanism may be related to the increase of serum and tissue HSP70 levels and inhibition of JNK signaling pathway.更多还原