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目的观察链脲佐菌素(STZ)诱导的糖尿病大鼠缺血/再灌注(I/R)模型心肌细胞凋亡及相关基因的表达。方法采用STZ(45 mg/kg)诱导大鼠糖尿病4周后制备心肌缺血30 min再灌注120 min模型,用2,3,5-氯化三苯基四氮唑染色法(TTC)测定心肌梗死面积,用TUNEI法检测细胞凋亡,用免疫组化方法检测凋亡相关基因的表达,透射电镜观察心肌组织超微结构的凋亡改变。结果与非糖尿病组相比,糖尿病组大鼠由I/R损伤引起的心肌梗死面积并没有增加,但是细胞凋亡指数增加(17%±3%比26%±3%,P<0.001)、Bcl-2表达降低(11.0%±3.8%比3.8%±2.5%,P<0.001)、Bax表达升高(26%±3%比36%±7%,P<0.001)、超微结构观察心肌凋亡损伤更为严重。结论糖尿病大鼠I/R心肌细胞凋亡增加,这可能与凋亡相关基因Bcl-2表达降低、Bax表达升高有关。
Objective To observe the cardiomyocyte apoptosis and related gene expression of streptozotocin (STZ) -induced diabetic rat model of ischemia / reperfusion (I / R). Methods The diabetic rats were induced by STZ (45 mg / kg) for 4 weeks, then the models of myocardial ischemia for 30 min and reperfusion for 120 min were prepared. The myocardium was measured by TTC (2,3,5,5-triphenyltetrazolium chloride) The area of infarct was detected by TUNEI method. The expression of apoptosis related gene was detected by immunohistochemistry. The ultrastructure of myocardium was observed by transmission electron microscope. Results Compared with non-diabetic group, the area of myocardial infarction induced by I / R injury in diabetic rats was not increased, but the apoptotic index increased (17% ± 3% vs 26% ± 3%, P <0.001) Bcl-2 expression was decreased (11.0% ± 3.8% vs 3.8% ± 2.5%, P <0.001), and Bax expression was higher (26% ± 3% vs 36% ± 7%, P <0.001) Apoptosis is more serious. Conclusion The apoptosis of I / R cardiomyocytes in diabetic rats increased, which may be related to the decrease of Bcl-2 expression and the increase of Bax expression.