冠心病心绞痛寒凝血瘀证大鼠心肌细胞凋亡及Bax、Bcl-2蛋白表达

目的:探讨冠心病心绞痛寒凝血瘀证大鼠心肌细胞凋亡及Bax、Bcl-2蛋白表达情况。方法:采用垂体后叶素大剂量静脉注射建立冠心病心绞痛寒凝血瘀证动物模型,运用TUNEL法检测细胞凋亡凋亡指数;免疫组化法检测心肌Bax、Bcl-2蛋白的表达;透射电镜观察大鼠心肌细胞的超微结构改变。结果:与正常组相比,模型组大鼠心肌细胞凋亡指数显著升高(P<0.05),Bax蛋白表达显著增加(P<0.01),Bcl-2蛋白表达无明显变化,Bax/Bcl-2显著升高(P<0.01),透射电镜下可见部分心肌细胞核固缩,染色质边集,线粒体聚集、肿胀,部分膜破裂,嵴降解。结论:心肌细胞凋亡参与了冠心病心绞痛寒凝血瘀证心肌缺血损伤的病理过程,Bax/Bcl-2表达失衡激活线粒体途径参与了冠心病心绞痛寒凝血瘀证心肌细胞凋亡的调控。

Myocardial Apoptosis and Expressions of Bax and Bcl-2 in Rats of Angina Pectoris with Syndrome of Congealing Cold with Blood Stasis

Objective ： To explore the myocardial apoptosis and expressions of Bax and Be1 - 2 in rats of angina pectoris with syndrome of congealing cold with blood stasis. Methods ： The animal model of angina pectoris with syndrome of con- gealing cold with blood stasis was established in rats by single high - dose intravenous injection of pituitrin. The apoptotic index, the expressions of Bax and Bcl - 2, and the uhramicrostructure of the myocardium were respectively determined by terminal deoxynucleotide transferase - mediated dUTP nick - end labeling （TUNEL） assays immunohistochemical staining and transmission electron microscopy. Results ： Compared with normal group, the apoptosis index, the expressions of Bax and the ratio of Bax/Bcl - 2 in model group were significantly increased （P 〈 0. O1 ）. Karyopyknosis and margination of the chromatin in some myocardial cells were observed under transmission electron microscopy. The mitochondria of some myocardial cells were congregated and swollen with some ruptured mitochondrial membrane and disrupted mitochondrial ridge. Conclusion ： An animal model of angina pectoris with syndrome of congealing cold with blood stasis was established successfully after analysis of ratg general conditions and microcosmic indexes. The myocardial apoptosis was involved in the pathological process of myocardial ischemia injury of angina pectoris with syndrome of congealing cold with blood sta- sis. The ratio of Bax/Bcl - 2 was involved in regulating apoptosis of angina pectoris with syndrome of congealing cold with blood stasis by mitochondrial pathway.