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目的:探讨双益方改善2型糖尿病大鼠糖、脂代谢作用及其作用机制。方法:利用高脂饲料喂养结合STZ腹腔注射建立2型糖尿病大鼠模型,模型建立后随机分为2型糖尿病模型组(DM)、罗格列酮组(RM)、双益方组(SY),并设正常对照组(NC)。实验治疗4周后,观察治疗期间及治疗后大鼠的一般情况,检测大鼠糖耐量、糖化血红蛋白(HbA1c)、血脂、空腹血清胰岛素(Ins)。并用实时荧光定量PCR检测各组大鼠骨骼肌Glut4mRNA表达。结果:双益方组、罗格列酮组均可改善2型糖尿病大鼠一般状况,与模型组比较空腹血糖、餐后0.5h、2h血糖、糖化血红蛋白、血脂明显降低(P<0.05),血清胰岛素升高(P<0.01),但双益方组、罗格列酮组之间未见显著性差异。实时荧光定量PCR检测模型组骨骼肌Glut4mRNA表达下调,与正常对照组相比,差异有统计学意义(P<0.05)。双益方组、罗格列酮组Glut4mRNA表达均上调,与模型组比较,差异均有统计学意义(P<0.05)。结论:双益方组对2型糖尿病大鼠具有降糖、降脂的作用,其作用机制可能与胰岛细胞保护和改善胰岛素抵抗有关。
Objective: To investigate the effect of Shuangyi on improving glucose and lipid metabolism and its mechanism in type 2 diabetic rats. Methods: A rat model of type 2 diabetes mellitus was established by intraperitoneal injection of high fat diet and STZ. The models were randomly divided into 2 groups: diabetic model group (DM), rosiglitazone group (RM), Shuangyi prescription group (SY) , And set the normal control group (NC). Four weeks after the experimental treatment, the general conditions of rats during and after treatment were observed. The glucose tolerance, glycosylated hemoglobin (HbA1c), blood lipid and fasting serum insulin (Ins) in rats were observed. The expression of Glut4 mRNA in skeletal muscle of rats in each group was detected by real-time fluorescence quantitative PCR. Results: Compared with the model group, fasting blood glucose, postprandial 0.5h, postprandial blood glucose, glycosylated hemoglobin and blood lipid of Shuangyi prescription group and rosiglitazone treatment group all improved the general condition (P <0.05) Serum insulin increased (P <0.01), but there was no significant difference between Shuangyi prescription group and rosiglitazone treatment group. The expression of Glut4mRNA in skeletal muscle was down-regulated by real-time fluorescence quantitative PCR. Compared with the normal control group, the difference was statistically significant (P <0.05). Glut4mRNA expression in Shuangyi group and Rosiglitazone group were both up-regulated compared with model group (P <0.05). Conclusion: Shuangyi prescription can reduce blood sugar and lipid in type 2 diabetic rats. Its mechanism may be related to islet cell protection and improvement of insulin resistance.