摘要
目的:研究促红细胞生成素(EPO)缺血后给药对在体大鼠心肌缺血再灌注损伤的保护作用,并对其机制进行初步探讨.方法:以左冠状动脉前降支穿线结扎法制备SD大鼠心肌缺血模型,松开结扎线造成再灌注.将大鼠随机分成假手术(SHAM)组、缺血再灌注(IR)组、促红细胞生成素(EPO)组和促红细胞生成素+磷脂酰肌醇-3-激酶(PI3K)/Akt途径的高选择性阻断剂LY294002(EPO+LY)组.观察心电图Ⅱ导联心律失常发生情况;电镜观察心肌细胞超微结构;以TUNEL法检测细胞凋亡;RT-PCR测定bc1-2,bax及caspase3 mRNA含量.结果:EPO组心肌细胞超微结构损伤较轻,细胞凋亡减少,再灌注心律失常发生率降低,bax及caspase-3mR-NA降低,bcl-2mRNA增高.结论:EPO对大鼠心肌缺血再灌注损伤具保护作用,LY294002可以减弱EPO的作用,其作用机制与抑制心肌细胞的凋亡作用有关,PI3K/Akt通路参与了其信号转导.
AIM：To explore the effect of erythropoietin（EPO）on myocardial ischemia reperfusion injury in rats,discuss the mechanism involved.METHODS：Thirty-five SD rats were randomly divided into 4 groups：Sham operation group（group SHAM）,and 3 experimental groups（group IR,group EPO and group EPO＋LY）.The ischemia repersusion heart model was established by ligating the left anterior descending branch of coronary artery;EPO was administrated by intravenous between ischemia and reperfusion.The occurrence of arrhythmia in electrocardiogram of lead Ⅱwas observed.The change of cardiac ultrastructure were examed by transmission electron microscope.Myocardium cells apoptosis were estimated by TUNEL;bcl-2,bax and caspase3 mRNA transcription were detected by RT-PCR.RESULTS：EPO could lighten the destruction of cardic ultrastructure,lighten reperfusion arrhythmia;EPO could up-regulate the mRNA transcription of bcl-2,and down-regulate the mRNA transcription of bax and caspase-3,inhibit the apoptosis myocardium cells;LY294002 attenuated the effect of EPO.CONCLUSION：EPO could attenuate myocardial ischemia-reperfusion injury.The cardioprotection by EPO required the PI3K pathway.
出处
《第四军医大学学报》
北大核心
2009年第19期1894-1897,共4页
Journal of the Fourth Military Medical University
