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目的探讨桑精胶囊治疗2型糖尿病的分子机制。方法采用尾静脉注射小剂量链脲佐菌素加高脂高热量饮食喂养的方法建立2型糖尿病大鼠模型,将造模动物随机分为模型组、二甲双胍组和桑精胶囊组,另设正常组对照。药物干预8周后,检测各组大鼠抗氧化能力指标超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、一氧化氮(NO)等,同时采用免疫组化法检测胰腺Bax、Bcl-2蛋白表达水平。结果模型组大鼠抗氧化能力及Bax、Bcl-2蛋白表达与正常组比较差异均有统计学意义(P<0.05或P<0.01);药物干预后,二甲双胍组、桑精胶囊组与模型组比较,SOD、GSH-Px、NO及Bax、Bcl-2蛋白表达均明显改善(P<0.05或P<0.01),其中对SOD、GSH-Px的改善桑精胶囊组要优于二甲双胍组(P<0.01)。结论桑精胶囊对2型糖尿病的治疗效应可能与其改善2型糖尿病大鼠氧化应激和抑制胰岛β细胞凋亡有关。
Objective To explore the molecular mechanism of Sangjing Capsule in treating type 2 diabetes. Methods Rat model of type 2 diabetes was established by tail vein injection of low-dose streptozotocin plus high fat and high-calorie diet. The model animals were randomly divided into model group, metformin group and Sangjing capsule group. Group control. After 8 weeks of drug intervention, the indicators of antioxidant capacity of the rats in each group were tested for superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and nitric oxide (NO). And so on. Simultaneously, immunohistochemistry was used to detect the expression of Bax and Bcl-2 protein in the pancreas. Results The anti-oxidation ability and Bax and Bcl-2 protein expression in the model group were significantly different from those in the normal group (P<0.05 or P<0.01). After the drug intervention, metformin group, Sangjing capsule group and model group In comparison, SOD, GSH-Px, NO and Bax, Bcl-2 protein expression were significantly improved (P <0.05 or P <0.01), and the improvement of SOD, GSH-Px was superior to metformin group (P <0.05). <0.01). Conclusion The therapeutic effect of Sangjing Capsule on type 2 diabetes may be related to the improvement of oxidative stress and inhibition of islet β cell apoptosis in type 2 diabetic rats.