福辛普利对心肌缺血再灌注损伤心肌细胞的作用和对Bcl-2、Bax表达的影响

Effect of Fosinopril Pretreatment on Cardiomyocytes Apoptosis and Bcl-2 and Bax mRNA Expression in Rats Model of Ischemia-reperfusion

目的探讨福辛普利对大鼠心肌缺血再灌注模型心肌细胞凋亡及相关调控基因Bcl-2、Bax表达的影响及相关机制。方法24只动物随机分成假手术组(=8),缺血再灌注损伤组(=8)和福辛普利预处理组(=8),再灌注24h后处死动物。用透射电镜观察大鼠心肌超微结构的变化,TUNEL法检测心肌细胞凋亡,RT-PCR检测Bcl-2及Bax基因表达。结果电镜结果显示福辛普利的应用促使缺血再灌注大鼠心肌组织肌原纤维排列趋于恢复正常、线粒体肿大好转、细胞核和核仁显示良好,无细胞核变形,无胞核空洞样变及核固缩等现象。TUNEL显示福辛普利组细胞凋亡明显减少。缺血再灌注损伤24h后心肌组织Bcl-2基因表达较假手术组显著降低,而Bax基因表达则显著增高,福辛普利则可以逆转这种趋势。结论应用福辛普利能抑制心肌缺血再灌注损伤导致的心肌细胞凋亡,发挥心肌保护作用,从而缓解缺血再灌注损伤的发生发展。

Objective To investigate the effect of fosinopril pretreatment on cardiomyocytes apoptosis and Bcl- 2 and Bax mRNA expression in rats model ofischemia- reperfusion. Methods 24 rats were randomly grouped to sham group, ischemical reperfusion injury group and fosinopril pretreatment group （n=8/each group） After 24 h of reperfusion, Cardiomyocytes ultrastructural, apoptosis and the related Bcl-2 and Bax gene expression were observed respectively. Results Fosinopril pretreatment attenuated the injury ofcardiomyocytes evaluated by electron microscope. Apoptosis of eardiomyocytes was decreased and Bcl-2 gene expression was up regulated and Bax gene expression was down regulated in fosinopril pretreatment group compared with ischemical reperfusion injury group. Conclusion Fosinopril pretreatrnent could inhibit apoptosis in ischemical reperfusion injury.