凋亡相关蛋白bcl-2和bax在糖尿病大鼠主动脉中的表达及意义

Expression of Apoptosis-Related Proteins bcl-2 and bax in the Aortas of Early Diabetic Rats

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 study the relationship of early diabetic macrovasculopathy with apoptosis-relatod proteins. Methods 24 Wistar rats were averagely divided into two groups： normal control group and diabetic group. Diabetes model was established in experimental group by injection of 50 mg alloxan/kgBW via the tail vein. After 10 weeks experimental term, the expressions of proteins bcl-2 and bax in aortas were detected by immunohistochemistry. Results It was found that the thickness of topical tunica intima of aortas increased in diabetic rats. In each focus, the elastic lamina existed asymmetric thickness and some had fissures and abruptions. The SMCs in superficial lamella showed slight proliferation and disorganized arrangement. Compared with control group, the positive rate of bcl-2 expression was decreased in aorta of diabetic rats （15.660±4.363% vs 45.115±10.492%）, while the rate of bax （42.606±4.717% vs 16.864±4.348%） was increased （P〈0.01）. Conclusions The change of bcl-2/bax induced by hyperglycemia might play an important role in diabetic macrovasculopathy through the mechanism of apeptosis.