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目的:观察大鼠急性心肌梗死(AM I)后的心肌细胞凋亡和caspase-3、Bc l-2和Bax表达的变化。方法:105只雌性SD大鼠,随机取78只结扎左冠状动脉建立AM I模型,24 h存活43只作为心肌梗死组(M I组);另27只设为假手术组(S组);两组再按观察时点随机分为48 h和4周两亚组,即:M I 48 h(n=11)和M I 4周(n=13)组,S48 h(n=10)和S4周(n=10)组。末端脱氧核糖核苷酸转移酶介导的dUTP切口末端标记技术(TUNEL)和DNA凝胶电泳检测心肌细胞凋亡。免疫组化方法和W estern b lotting检测caspase-3、Bc l-2和Bax的表达。结果:M I 48 h组动脉收缩压(SBP)、舒张压(DBP)、平均压(MAP)、左心室收缩压(LVSP)和左心室内压最大上升下降速率(±dp/dt)均显著低于S组(P<0.05,P<0.01),左心室舒张末压(LVEDP)显著高于S组(P<0.05);M I 4周组除SBP、DBP和MAP无显著差异(均P>0.05)外,上述其它指标的变化与M I 48 h组相同,且LVEDP升高更为显著(P<0.01);M I 48 h和4周两组梗死/疤痕区、梗死边缘区和非梗死区的心肌细胞凋亡指数均显著升高(P<0.05,P<0.01),心肌细胞中“凋亡执行因子”caspase-3和“凋亡促进基因”Bax的表达亦均显著增高(P<0.05,P<0.01),而“凋亡抑制基因”Bc l-2仅在M I 48 h组梗死区心肌细胞中表达增加,“抑制凋亡复合基因”Bc l-2/Bax的比值仅在M I 48 h组降低。结论:大鼠AM I后,梗死区及其边缘区和非梗死区均有心肌细胞凋亡发生,伴“凋亡执行因子”caspase-3和“凋亡促进基因”Bax的表达增加;AM I早期,“凋亡抑制基因”Bc l-2在梗死区表达增加,但“抑制凋亡复合基因”Bc l-2/Bax的比值下降。
Objective: To observe the changes of myocardial apoptosis and the expressions of caspase-3, Bcl-2 and Bax after acute myocardial infarction (AMI) in rats. Methods: A total of 105 female Sprague-Dawley rats were randomly divided into two groups: AM I model was established by ligating the left coronary artery, and 43 rats survived 24 h as myocardial infarction group (MI group); the other 27 rats were sham-operated group (S group) The rats were randomly divided into two subgroups: 48 h and 4 wk after MI 48 h (n = 11) and MI 4 (n = 13), S48 h (n = 10) and S4 n = 10) group. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and DNA gel electrophoresis were used to detect cardiomyocyte apoptosis. Immunohistochemistry and Western blotting were used to detect the expression of caspase-3, Bcl-2 and Bax. Results: SBP, DBP, MAP, LVSP and ± dp / dt in MI 48 h group were all significantly lower than those in control group LVEDP in S group was significantly higher than that in S group (P <0.05, P <0.01); there was no significant difference except SBP, DBP and MAP in MI 4 weeks group (all P> 0.05 ), The changes of other indexes mentioned above were the same as those of MI 48 h group, and the increase of LVEDP was more significant (P <0.01); myocardial infarct / scar area, infarct border area and non-infarct area myocardial MI (P <0.05, P <0.01). The expressions of caspase-3 and Bax were also significantly increased in cardiomyocytes (P <0.05, P <0.01). However, the expression of Bcl-2 was only increased in MI 48h MI group and the ratio of Bcl-2 / Bax in MI 48h group reduce. CONCLUSION: Myocardial apoptosis occurs in AMI, infarct area, borderline area and non-infarct area, and the expression of caspase-3 and Bax in “apoptosis-promoting gene” In the early stage, the expression of Bcl-2, an inhibitor of apoptosis, increased in the infarct zone but decreased in the Bcl-2 / Bax ratio of the apoptotic complex.