CAJ | 학술논문

目的:观察缺血后处理对大鼠心肌缺血再灌注损伤后心肌梗死面积及心肌细胞凋亡的影响,初步探讨其心肌保护的作用机制.方法:36只健康雄性Wistar大鼠(230～280 g)随机平均分为3组,缺血再灌注(I-R)组,缺血后处理(Post)组,缺血后处理+ AG490(JAK2-STAT3通路阻断剂)组(Post+AG490组).I-R组缺血30 min, 再灌注120 min. Post组缺血30 min,再灌注120 min,并于再灌注前实施缺血后处理(灌注10 s,缺血10 s) 3个循环.Post+AG490组再灌注前5 min静脉注射AG490,其他处理与Post组相同.再灌注120 min后取心肌标本.TTC染色法检测心肌梗死面积;TUNEL法测定心肌细胞凋亡指数.结果:缺血后处理组与对照组相比心梗面积及心肌细胞凋亡指数明显降低(P ＜ 0.05).AG490抑制了缺血后处理的心肌保护作用.结论:缺血后处理具有显著的心肌保护作用,这一作用是由JAK2-STAT3通路介导的.
목적:관찰결혈후처리대대서심기결혈재관주손상후심기경사면적급심기세포조망적영향,초보탐토기심기보호적작용궤제.방법:36지건강웅성Wistar대서(230～280 g)수궤평균분위3조,결혈재관주(I-R)조,결혈후처리(Post)조,결혈후처리+ AG490(JAK2-STAT3통로조단제)조(Post+AG490조).I-R조결혈30 min, 재관주120 min. Post조결혈30 min,재관주120 min,병우재관주전실시결혈후처리(관주10 s,결혈10 s) 3개순배.Post+AG490조재관주전5 min정맥주사AG490,기타처리여Post조상동.재관주120 min후취심기표본.TTC염색법검측심기경사면적;TUNEL법측정심기세포조망지수.결과:결혈후처리조여대조조상비심경면적급심기세포조망지수명현강저(P ＜ 0.05).AG490억제료결혈후처리적심기보호작용.결론:결혈후처리구유현저적심기보호작용,저일작용시유JAK2-STAT3통로개도적.
Objective: To investigate the effect of ischemic postconditioning on myocardial infarction and myocardial apoptosis in ischemia-reperfusion injury of rats, and the protective mechanisms thereof. Methods:Thirty-six healthy male Wistar rats(230-280 g) were randomly divided into three groups, ischemia-reperfusion group(Group I-R), ischemia 30 min and reperfusion 120 min without additional intervention; myocardial ischemic postconditioning group(Group Post), after 30 min ischemia, the rats were comprised 3 cycles of 10 seconds reperfusion followed by 10 seconds ischemia, and then the rats were reperfused 120 min; myocardial ischemic postconditioning+AG490(JAK2-STAT3 pathway inhibitor) group(Group Post+AG490), rats were treated with AG490 5 minutes before reperfusion, followed by myocardial ischemic postconditioning and 120 min reperfusion. The myocardial infarct size was measured by TTC staining. Apoptotic index of cardiomyocyte was detected by TUNEL. Results: Myocardial infarct size and myocardium apoptotic index were significantly reduced in Group Post compared to those in Group I-R(P ＜ 0.05). AG490 inhibited cardioprotective effect of ischemic postconditioning. Conclusion: Ischemic postconditioning provides potent cardioprotective effect. JAK2-STAT3 pathway mediates the cardioprotective effects of ischemic postconditioning.