凋亡基因在心肌梗死的表达及血管紧张素转化酶抑制剂的干预作用

Expression of apoptosis-related genes in rats with myocardial infarction and effects of ACEI

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 expression of apoptosis- related genes in rats with myocardial infaretion and effects of ACEI. Methods Twenty-four rats were randomly divided into four groups ; sham operated greup,MI model group,MI model plus low-dosage fosinopril group, MI model plus high-dosage fosinopril group .After 24 hours and 4 weeks Bcl-2, Bax, Fas, P53 mRNA expression were measured by reverse transcription PCR. Rcsults After 24 hours Bcl-2 mRNA expression were lower,fosinopril enhanced its over expression,Bax, Fas, P53 mRNA expression were higher,fosinopril inhibited their expression.After 4 weeeks in MI model group Bcl-2 mRNA expression were lower, fosinopril enhanced its expression,Bax,P53 mRNA expression were invariant,fosinopril had no effects,Fas mRNA expression were higher, fosinopril inhibited its expression. Conclusion Myocyte apoptosis may play a pivotal role in MI,the suppression of Bcl-2 and the over expression of Bax,P53,Fos induce signal pathways of cardiomyeeyte apoptosis, ACEI inhibits the cardiomyeeyte apoptosis by effects of these genes.