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目的探讨凋亡基因对大鼠心肌梗死的表达及血管紧张素转化酶抑制剂(ACEI)的干预作用。方法将大鼠随机分为假手术组、梗死模型组、梗死模型+福辛普利小剂量组、梗死模型+福辛普利大剂量组,用逆转录-聚合酶链反应(RT-PCR)方法检测大鼠心肌梗死24h和4周时心肌细胞内凋亡抑制基因Bcl-2与凋亡基因Bax、P53、Fas的mRNA表达量,并探讨它们之间的相互关系。结果急性心肌梗死24hBcl-2表达下降,福辛普利促进其高表达,Bax、P53、Fas增高,福辛普利抑制其表达;急性心肌梗死4周,Bcl-2表达下降,福辛普利促进其表达,Bax、P53表达变化不大,福辛普利对其表达无影响,Fas高表达,福辛普利抑制其表达。结论大鼠急性心肌梗死后心肌细胞存在凋亡现象,Bcl-2表达下降,Bax、P53、Fas表达上调介导心肌梗死后心肌细胞凋亡的发生。ACEI可通过干预上述基因抑制急性心肌梗死后的心肌细胞凋亡。
Objective To investigate the effect of apoptosis gene on myocardial infarction and angiotensin-converting enzyme inhibitor (ACEI) in rats. Methods The rats were randomly divided into 4 groups: sham operation group, infarction model group, infarction model + fosinopril low dose group, infarction model + fosinopril high dose group, reverse transcription polymerase chain reaction (RT- Methods The mRNA expression of Bcl-2 and Bax, P53 and Fas in cardiomyocytes were detected at 24 and 4 weeks after myocardial infarction in rats, and the relationship between them was explored. Results Fosinopril promoted the expression of Bcl-2 at 24 h after AMI, and increased the expression of Bax, P53 and Fas, while inhibited the expression of Bcl-2 at 4 weeks after AMI. Fosinopril Promote the expression of Bax, P53 little change, Fosinopril had no effect on its expression, Fas high expression, Fosinopril inhibited its expression. Conclusion The apoptosis of myocardial cells after acute myocardial infarction in rats is observed. The expression of Bcl-2 is down-regulated. The up-regulation of Bax, P53 and Fas induces cardiomyocyte apoptosis after myocardial infarction. ACEI can inhibit cardiomyocyte apoptosis after acute myocardial infarction by intervening these genes.