罗格列酮对2型糖尿病大鼠心脏组织脂联素受体2单核趋化蛋白-1表达的影响

目的探讨罗格列酮对2型糖尿病大鼠心脏组织中脂联素受体2(AdipoR2)、单核趋化蛋白(MCP)-1表达影响。方法 36只雄性Wistar大鼠,随机分为3组:健康对照组(A组,10只),糖尿病组(B组,13只)和罗格列酮治疗组(C组,13只),采用高糖高脂饮食加小剂量链脲佐菌素(STZ)的方法诱导糖尿病模型。用反转录-聚合酶链反应(RT-PCR)的方法测定大鼠心肌AdipoR2mRNA、MCP-1mRNA的表达,用免疫组织化学法检测心脏组织中AdipoR2蛋白的表达。结果与A组比较,B组糖尿病大鼠心质量/体质量增加,MCP-1表达增加,血浆脂联素水平、心肌AdipoR2mRNA和蛋白表达显著降低。经罗格列酮治疗后,C组大鼠心质量/体质量、MCP-1mRNA降低,血浆脂联素水平、心肌AdipoR2mRNA和蛋白表达增加。结论 2型糖尿病大鼠心肌Adi-poR2表达水平降低,MCP-1的表达水平升高,罗格列酮上调2型糖尿病大鼠心肌AdipoR2的表达,并抑制MCP-1的过度表达从而延缓糖尿病心肌病的进展,可能是其心脏保护作用机制之一。

Effects of rosiglitazone on the expression of adiponectin receptor and monocyte chemotactic protein-1 in the heart tissue of type 2 diabetic rats

Objective To investigate the effect of rosiglitazone on the expression of adiponeetin receptor （Adi- poR2） and monocyte ehemotaetic protein （MCP）-1 in heart tissue of type 2 diabetic rats. Methods Thirty-six male Wistar rats were randomly divided into three groups： normal control group （group A, n =10）, diabetic group （group B, n =13） and rosiglitazone-treated diabetic group （group C, n=13）. High-fat and high-sugar diets plus a low dose injection of streptozotocin （STZ） were performed to rats for establishing diabetic models. The expression of myocardial Adi- poR2 mRNA and MCP-I mRNA were measured by RT-PCR, and protein expression of myocardial AdipoR2 was detected by immunohistoehemieal staining. Results Compared with rats from group A, those from group B were heavier with a higher ratio of heart to body and an increased MCP-1 expression, while their expression of plasma adiponectin, cardiac AdipoR2 mRNA and protein significantly decreased. With rosiglitazone, rats in group C showed a decreased ratio of heart to body weight and decreased MCP-1 mRNA expression, increased plasma adiponeetin and increased protein and mRNA expression of myocardial AdipoR2 （protein and mRNA）. Conclusion In type 2 diabetic rats treated by rosiglitazone, the expression of AdipoR2 degraded, and the expression of MCP-1 upgraded, showing that rosigli- tazone may upgrade the expression of AdipoR2 and inhibit MCP-1 over-expression, through which way, the progress of diabetic cardiomyopathy may be deferred, and this may be one of the cardioprotective mechanisms.