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目的观察罗格列酮对实验性2型糖尿病大鼠肝脏组织中IRS-2表达的调节,进一步探讨其可能的作用机制。方法采用低剂量链脲佐菌素尾静脉注射联合高脂饲料喂养建立2型糖尿病大鼠模型。未予上述处理的大鼠作为正常对照组(NC组),成模大鼠随机分为糖尿病对照组(UD组)和罗格列酮干预组(RI组)。药物干预4周后,称重,检测血清葡萄糖、胰岛素、甘油三酯和胆固醇,检测大鼠肝脏组织中IRS-2蛋白及mRNA的表达。结果(1)RI组大鼠空腹血糖、胰岛素、甘油三酯水平均低于UD组(P<0.05),高于NC组(P<0.05);RI组血清胆固醇高于NC组(P<0.05),与UD组差异无显著性(P=0.318);(2)免疫印记法示:UD组与NC组相比,肝脏IRS-2蛋白表达明显减少,RI组肝脏IRS-2蛋白表达增加,介于前两者之间,差异均有显著性(P<0.05)。RT-PCR示,UD组较NC组肝脏IRS-2mRNA表达下调,而RI组IRS-2mRNA表达水平介于二者之间。结论IRS-2的继发性减少可能是2型糖尿病的发病机制之一;罗格列酮能够上调IRS-2mRNA及蛋白的表达,这可能是其改善胰岛素抵抗、保护胰岛β细胞的另一作用机制。
Objective To observe the regulation of rosiglitazone on the expression of IRS-2 in the liver tissue of experimental type 2 diabetic rats and to explore its possible mechanism. Methods Low-dose streptozotocin (STZ) was injected into tail vein of rats and fed with high fat diet to establish type 2 diabetic rat model. The rats without the above treatment as the normal control group (NC group), the model rats were randomly divided into diabetic control group (UD group) and rosiglitazone intervention group (RI group). Four weeks after drug intervention, serum glucose, insulin, triglyceride and cholesterol were measured and the expression of IRS-2 protein and mRNA in rat liver tissue were measured. Results (1) The levels of fasting blood glucose, insulin and triglyceride in RI group were lower than those in UD group (P <0.05), and higher in RI group than those in NC group (P <0.05) (P = 0.318). (2) Immunofluorescence showed that the expression of IRS-2 protein in liver was significantly decreased in UD group compared with NC group, and the expression of IRS-2 protein in RI group was increased, Between the first two, the differences were significant (P <0.05). RT-PCR showed that IRS-2mRNA expression was down-regulated in UD group compared with NC group, while IRS-2mRNA expression level in RI group was in between. Conclusions The secondary decrease of IRS-2 may be one of the pathogenesis of type 2 diabetes. Rosiglitazone can up-regulate the expression of IRS-2 mRNA and protein, which may be another role of insulin resistance and protection of islet β-cell mechanism.