芪丹通脉片对缺血/再灌注大鼠心肌细胞凋亡及相关基因Bcl-2与Bax表达的影响

Study of the Effect of Qidantongmai Tablet on Reperfusion-induced Myocardial Apoptosis and the Expression of Bcl-2 and Bax in rats

目的观察芪丹通脉片对缺血/再灌注大鼠心肌细胞凋亡及相关基因Bcl-2和Bax表达的影响。方法雄性SD大鼠随机分为假手术组、模型组、不同剂量芪丹通脉片组,分组干预7d后,通过结扎冠状动脉左降支40min后再灌注4h成功复制心肌I/RI模型。TUNEL法检测心肌凋亡细胞,免疫组化检测Bcl-2和Bax蛋白的表达。结果不同剂量芪丹通脉片(1.08,3.24g/kg)预处理可抑制I/RI中心肌细胞凋亡,其凋亡指数分别为(14.3±3.8)%和(10.6±2.0)%,与模型组(21.3±4.2)%比较均存在显著差异。模型组Bcl-2平均灰度值为(165.17±9.21);不同剂量芪丹通脉片(1.08,3.24g/kg)预处理后缺血/再灌注心肌组织中Bcl-2的平均灰度值分别为(147.82±19.51)和(118.65±16.31),平均灰度较模型组明显降低;模型组Bax平均灰度值为(139.43±11.70),芪丹通脉片(1.08,3.24g/kg)预处理后Bax-2的平均灰度值分别为(151.67±16.69)和(160.71±19.82),二者的灰度值与模型组比较有降低,但无显著差异。结论芪丹通脉片能抑制缺血/再灌注所致的心肌细胞凋亡,其机制与调节再灌注心肌中Bcl-2、Bax的表达有关。

Objective： To investigate the effect of Qidantongmai Tablet（QDTMT） on myocardial apoptosis and the expression of Bcl -2 and Bax in heart tissue from rats subjected to reperfusion injury. Methods： Male Spragne - Dawley（SD） rats were divided randomly into 4 groups： Sham, ischemia/reperfusion（control）, QDTMT- I（ 1.08g/ kg）treatment and QDTMT - Ⅱ（3.24g/kg）treatment. The rats were anesthetized and subjected to 40 min occlusion of left descending coronary artery followed by 4h reperfusion. The cardiomyocyte apoptosis was determined by terminal deoxynucleotidy transfease - mediated dUTP nick - end labeling（TUNEL） . The expressions of Bcl - 2 and Bax in heart tissue were assessed by immunohistochemical stain. Results： The mean grey level of Bcl - 2 or Bax decreased significantly in control compared with sham. The mean grey levels of Bcl - 2 in the group of in vivo perconditioning of QDTMT at doses of I. 08 g/kg and 3.24g/kg orally for 7d were significantly lower than the level in control. The mean grey levels of Bax in the groups of the preconditioning of QDTMT at dosages of 1.08g/kg and 3.24 g/kg decreased slightly, which were no significantly lower than the level in control. Conclusion： The result indicated that the treatment of QDTMT could attenuate reperfusion - induced myocardial apoptosis in rat heart, which is possibly related to moduation of the a the expressions of anti - apoptosis protemin and pro - apoptosis protein.