CAJ | 학술논문

目的：：探讨钙蛋白酶在小鼠心肌缺血/再灌注( Ischemia/Reperfusion,I/R)损伤中的作用。方法：采用结扎/松解左冠状动脉前降支的方法建立小鼠心肌I/R模型。将实验动物随机分为假手术组、I/R组(冠状动脉结扎45 min,再灌注3 h)及PD+I/R组( I/R前30 min静脉注射钙蛋白酶抑制剂-PD1506061 mg/kg)。再灌注结束后,测定各组心肌梗死面积、细胞色素C含量、caspase-3活性。结果：与I/R组相比,PD150606预处理组心肌梗死区域面积明显减小,且PD150606能明显抑制由I/R引起的细胞色素C含量及caspase-3活性增加。结论：钙蛋白酶活化介导的心肌细胞凋亡在小鼠心肌I/R损伤中发挥了重要的作用。
목적：：탐토개단백매재소서심기결혈/재관주( Ischemia/Reperfusion,I/R)손상중적작용。방법：채용결찰/송해좌관상동맥전강지적방법건립소서심기I/R모형。장실험동물수궤분위가수술조、I/R조(관상동맥결찰45 min,재관주3 h)급PD+I/R조( I/R전30 min정맥주사개단백매억제제-PD1506061 mg/kg)。재관주결속후,측정각조심기경사면적、세포색소C함량、caspase-3활성。결과：여I/R조상비,PD150606예처리조심기경사구역면적명현감소,차PD150606능명현억제유I/R인기적세포색소C함량급caspase-3활성증가。결론：개단백매활화개도적심기세포조망재소서심기I/R손상중발휘료중요적작용。
Objective: To determine whether and how calpain involved in ischemia/reperfusion( I/R)-injury. Methods:Liga-tion and release of the left coronary artery was performed to establish mouse myocardial I/R-injury models. Mice were randomly divided into Control group,I/R group and PD+I/R group. Triphenyltetrazolium chloride ( TTC) stain was employed to observe the myocardial infarction area in different groups. The level of Cytochrome C and the activity of caspase-3 were also detected. Results:Calpain inhibitor PD150606 significantly reduced the myocardial infarction area caused by I/R. Moreover,we found the level of Cytochrome C and the ac-tivity of caspase-3 were significantly increased in I/R group compared with Control group. However, these changes were blunted by PD150606;the increase of Cytochrome C level and caspase-3 activity was inhibited in PD+I/R group. Conclusion:Calpain mediated cardiac myocytes apotosis plays an important role in myocardial I/R-injury of mouse.