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目的探讨糖尿病大鼠早期大血管病变中凋亡相关蛋白bcl-2和bax表达的变化及意义。方法选用Wistar大鼠,随机分为正常对照组和糖尿病组,每组12只。以四氧嘧啶50mgk/g尾静脉注射制造糖尿病模型。10周后,免疫组化染色观察主动脉中凋亡相关蛋白bcl-2及bax蛋白表达情况。结果糖尿病大鼠主动脉表现为局限性内膜增厚,中膜浅层平滑肌细胞轻度增生、排列紊乱、病灶处内弹力板呈波浪状或交织状排列、有断裂分离现象。糖尿病组与对照组相比,主动脉bcl-2蛋白表达下降,而bax蛋白表达增加,差别有统计学意义(均P<0.01)。结论高血糖可能诱导的bcl-2b/ax比例下降,促进血管内皮及平滑肌细胞凋亡,参与糖尿病大血管病变的发生发展。
Objective To investigate the changes of apoptosis-related proteins (bcl-2 and bax) in early stage of diabetic macrovascular complications and its significance. Methods Wistar rats were randomly divided into normal control group and diabetic group, 12 rats in each group. Alloxan 50mgk / g tail vein injection to create a diabetic model. After 10 weeks, the expressions of bcl-2 and bax protein in the aorta were observed by immunohistochemistry. Results The aorta in diabetic rats showed localized thickening of the intima and mild proliferation of smooth muscle cells in the tunica media with disordered arrangement. The elastic plates in the lesion were arranged in a wavy or intertwined pattern with the phenomenon of fracture and separation. Compared with the control group, the bcl-2 protein expression and the bax protein expression in aortas of diabetic group were significantly decreased (all P <0.01). Conclusion Hyperglycemia may decrease the ratio of bcl-2b / ax and promote the apoptosis of vascular endothelial cells and smooth muscle cells, which may be involved in the occurrence and development of diabetic macroangiopathy.