| 钙蛋白酶活化在小鼠心肌缺血再灌注损伤中的作用 |
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| 引用本文： | 张双,徐磊,岳荣川,张辉,王欢,陈海燕,谭春燕,张荣驿,倪海燕. 钙蛋白酶活化在小鼠心肌缺血再灌注损伤中的作用[J]. 川北医学院学报, 2015, 0(2): 144-146. DOI: 10.3969/j.issn.1005-3697.2015.02.03 |
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| 作者姓名： | 张双 徐磊 岳荣川 张辉 王欢 陈海燕 谭春燕 张荣驿 倪海燕 |
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| 作者单位： | 1. 什邡市人民医院心内科，四川 什邡 618400; 川北医学院附属医院心内科，四川 南充 637000;2. 川北医学院附属医院心内科,四川 南充,637000;3. 什邡市人民医院心内科,四川 什邡,618400 |
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| 摘 要： | 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3h)及PD+I/R组(I/R前30 min静脉注射钙蛋白酶抑制剂-PD150606 1 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。
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| 关 键 词： | 钙蛋白酶 缺血/再灌注 凋亡 |
Effects of calpain activation in myocardial ischemia/reperfusion injury of mouse |
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| ZHANG Shuang,XU Lei,YUE Rong-chuan,ZHANG Hui,WANG Huan,CHEN Hai-yan,TAN Chun-yan,ZHANG Rong-yi,NI Hai-yan. Effects of calpain activation in myocardial ischemia/reperfusion injury of mouse[J]. Journal of North Sichuan Medical College, 2015, 0(2): 144-146. DOI: 10.3969/j.issn.1005-3697.2015.02.03 |
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| Authors: | ZHANG Shuang XU Lei YUE Rong-chuan ZHANG Hui WANG Huan CHEN Hai-yan TAN Chun-yan ZHANG Rong-yi NI Hai-yan |
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| Affiliation: | ZHANG Shuang;XU Lei;YUE Rong-chuan;ZHANG Hui;WANG Huan;CHEN Hai-yan;TAN Chun-yan;ZHANG Rong-yi;NI Hai-yan;Department of Cardiology,People’s Hospital of Shifang;Department of Cardiology,Affiliated Hospital of North Sichuan Medical College; |
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| Abstract: | 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. |
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| Keywords: | Calpain Ischemia/reperfusion Apotosis |
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