摘要
目的探讨抑郁对急性心肌梗死后大鼠心肌细胞凋亡的影响。方法 30只SD大鼠随机分为三组,假手术组,心肌梗死对照组,心肌梗死抑郁组,每组10只。制备相应模型并干预后,用TUNEL法检测心肌细胞凋亡,用免疫组织化学法检测心肌细胞Bcl-2、Bax蛋白的表达。结果心肌梗死抑郁组和心肌梗死对照组大鼠心肌细胞凋亡率以及心肌细胞Bcl-2、Bax蛋白表达均高于假手术组,差异有统计学意义(P<0.01),心肌梗死抑郁组大鼠心肌细胞凋亡指数以及心肌细胞Bax蛋白表达高于心肌梗死对照组,而心肌细胞Bcl-2蛋白表达低于心肌梗死对照组,差异有统计学意义(P<0.01)。结论抑郁可增加急性心肌梗死大鼠心肌细胞凋亡,其机制可能与促进促凋亡基因Bax表达、抑制抗凋亡基因Bcl-2表达有关。
Objective To explore the effects of depression on cardiac myocyLe apoptosis in rats with acute myocardial infarction （AMI）. Methods 30 Rats were randomly divided into three groups： Sham-operated group （n = 10）, AMI group （n = 10）, AMI de- pression group （n = 10）. After establishment of model and intervention, apoptosis of cardiac myocyte was detected with TUNEL method, and the expression of Bcl-2 and Bax were examined with immunohistochemistry method. Results The apoptosis indexes of cardiac myocyte and the expression levels of Bcl-2, Bax in AMI group and AMI depression group were higher than Sham-operated group, the difference was statistically significant （P 〈 0.01 ）. The apoptosis indexes of cardiac myocyte and the expression levels of Bax in AMI depression group was higher than AMI group, while the expression levels of Bcl-2 were lower than AMI group, the differ- ence was statistically significant （ P 〈 0.01 ）. Conclusions Depression could increase cardiac myocyte apoptosis in rats with AMI, and the mechanism mac be associated with up-regulating expression of Bax and down-regulating expression of Bcl-2.
出处
《心脑血管病防治》
2015年第6期457-458,共2页
CARDIO-CEREBROVASCULAR DISEASE PREVENTION AND TREATMENT
