Bcl-2和Bnip-3在糖尿病性心肌病大鼠心肌细胞中的表达

目的探讨细胞凋亡因子Bcl-2、Bnip-3在实验性糖尿病性心肌病大鼠心肌细胞中的表达情况。方法选取8周龄Sprague-Dawley大鼠30只,随机分为对照组和模型组。对照组大鼠腹腔注射枸橼酸缓冲液,模型组大鼠一次性腹腔注射链脲佐菌素溶液建立糖尿病模型,继续饲养12周,自然形成糖尿病性心肌病模型;然后处死2组大鼠,取血测定血糖、血脂,取心脏称质量计算心脏质量指数,切取心肌组织电镜观察心肌超微结构变化,并测定乳酸脱氢酶(LDH)和肌酸激酶(CK)水平,免疫组织化学法测定心肌细胞Bcl-2、Bnip-3的表达。结果模型组大鼠血糖、三酰甘油、胆固醇、高密度脂蛋白、低密度脂蛋白、心肌酶及心肌形态学改变均符合糖尿病性心肌病表现。模型组大鼠心肌细胞中Bcl-2的表达明显低于对照组(P<0.01),Bnip-3的表达明显高于对照组(P<0.01)。结论细胞凋亡因子Bcl-2和Bnip-3可能参与了糖尿病性心肌病的心肌细胞凋亡过程。

Expression of Bcl-2 and Bnip-3 in myocardial cell of diabetic cardiomyopathy rats

Objective To explore the expressions of Bcl-2 and Bnip-3 in myocardial cell of experimental diabetic cardiomyopathy（DCMP） rats. Methods Eight weeks Sprague-Dawley （SD）rats were randomly divided into control group and model group. SD rats of control group received citric acid buffer solution peritoneal injection. The DCMP models were estoblished by injecting streptozotocin（STZ） solution in rats of model group ,than the rats were continued to raise 12 weeks ,the models of the DCMP were formed naturally. All rats were sacrificed. Blood glucose, lipid profile were determined, heart were weighed to calculate cardiac weight index. Myocardial tissue was performed to observe ultrastructure changes with electron mi- croscope;the levels of lactate dehydrogenase（ LDH）, creatine kinase （CK）in myocardial tissue were determined. The expres- sion levels of Bcl-2 and Bnip-3 in myocardial cell were measured by immunohistochemical method. Results The changes of blood chemistry indexes including blood glucose, triacylglycerol, cholesterin, high density lipoprotein, low density lipoprotein, myocardial enzyme and myocardial morphology all conformed to the features of DCMP. The expression of Bcl-2 in myocardial cell of model group was obviously lower than that of control group （P 〈 0.01 ）, while the expression of Bnip-3 in myocardial cell of model group was obviously higher than that of control group （ P 〈 0.01 ）. Conclusion Apoptosis factors Bcl-2 and Bnip-3 in myocardial cell may take part in the diabetic myocardial damage processes.