摘要
目的研究促红细胞生成素(EPO)对大鼠心肌缺血再灌注损伤(I／R)的延迟保护作用。方法将60只SD大鼠随机分成空白对照组(A组)、1 000 U／kg EPO预处理组(B组)和3 000 U／kg EPO预处理组(C组),B、C组均提前24 h腹腔注射EPO。建立Langendorff大鼠离体心脏灌注模型,各组分别平衡灌注20 min后,缺血30 min,再复灌45 min。复灌20 min后测定并比较冠状动脉流液中磷酸肌酸激酶(CK)和乳酸脱氢酶(LDH)的含量;实验结束后,电子显微镜下观察各组心肌细胞超微结构的变化,并通过免疫组织化学法检测凋亡相关基因bax、bcl-2的蛋白表达。结果复灌20 min后,B、C组CK和LDH漏出量分别为(11．58±2．05)U／L、(16．24±2．02)U／L和(10．34±1．56)U／L、(15．16±2．67)U／L,均显著低于A组的(27．22±2．14)U／L和(29．12±1．45)U／L(P值均<0．05)。实验结束后,B、C组心肌细胞超微结构损伤显著减轻。B、C组Bax阳性片数率分别为50％和30％,均显著低于A组的95％(P值均<0．05),C组亦显著低于B组(P<0．05)。B、C组Bcl-2阳性片数率分别为35％和70％,均显著高于A组的20％(P值均<0．05),C组亦显著高于B组(P< 0．05)。结论EPO对大鼠心肌I／R具延迟保护作用,其作用机制与抑制心肌细胞的凋亡有关。
Objective To assess the delayed protective effects of erythropoietin（EPO） in isolated rat myocardium against ischemia and reperfusion injury （I/R）. Methods Sixty SD rats were randomly divided into control group （group A）, and two experimental groups （group B,group C） in the latter 2 with intraperitoneal injection of 1 000 U/kg and 3 000 U/kg of EPO 24 hours before I/R. Langendorff model of isolated rat heart was constructed and followed by a 3-stage protocol, 20 min preperfusion, 30 min ischemia, and 45 min reperfusion. Creatine phosphokinase isoenzyme（CK） and lactate dehydrogenase（LDH） in the coronary effluents were measured; the changes of myocardial ultrastructures were observed under electronmicropscopy, and immunohischemistry was used to study the apoptosis-related gene expression of bcl-2, bax at protein levels. Results EPO reduced CK. LDH in the coronary effluent attenuated the injury of myocardial ultrastructures, up-regulated the expression of Bcl-2, and downregulated the Bax expression; the effects were relatively dose-dependent. Conclusion EPO pretreatment has delayed protective effects on the isolated rat hearts against I/R, and its mechanism of action is related with inhibition of apoptosis. （Shanghai Med J, 2007, 30 ： 121-123）
出处
《上海医学》
CAS
CSCD
北大核心
2007年第2期121-123,F0003,共4页
Shanghai Medical Journal
