设为首页
加入收藏
联系我们
Email-Alert
 

    首页 | 杂志介绍 | 编委成员 | 审稿专家名录 | 投稿指南 | 订阅指南 | 过刊浏览 | 广告投放 | 论著模板 | 综述模板 | 帮助

 
项 洁,吴 鑫,陆 晓,励建安.心肌远隔缺血预适应通过SDF-1α/CXCR4途径保护兔心肌缺血/再灌注损伤的研究[J].中国康复医学杂志,2017,(10):1101~1107
心肌远隔缺血预适应通过SDF-1α/CXCR4途径保护兔心肌缺血/再灌注损伤的研究    点此下载全文
项 洁  吴 鑫  陆 晓  励建安
徐州医科大学附属医院康复医学科,江苏徐州,221000
基金项目:国家自然科学基金面上项目(81472164);徐州市社会发展项目(XM13B060)
DOI:
摘要点击次数: 65
全文下载次数: 46
摘要:
      摘要 目的:探讨远隔缺血预适应对心肌缺血/再灌注(I/R)损伤保护作用及潜在机制。 方法:成年雄性新西兰大白兔随机分成:①心肌缺血再灌注组(I/R组,n=6);②假手术组(Sham,n=6);③远隔缺血预适应(RIPC+I/R组,n=6);④SDF-1α/CXCR4阻断剂AMD3100+I/R组,(n=6);⑤AMD3100+RIPC+I/R组,(n=6)。ELISA检测外周血中SDF-1α;TTC检测心肌梗死面积;TUNEL检测细胞凋亡率;Western Blot检测Bcl-2、Bax蛋白表达。 结果:与Sham组相比,I/R组及RIPC+I/R组都可促进外周血中SDF-1α的释放,且后者的作用更显著(P<0.05);RIPC+I/R及AMD3100+RIPC+I/R组可以不同程度缩小心肌梗死面积及降低心肌细胞凋亡率(P<0.05),AMD3100+RIPC+I/R组与RIPC+I/R组相比,心肌梗死面积及细胞凋亡率均有所增加(P<0.05)。 结论:远隔缺血预适应可能通过SDF-1α/CXCR4信号通路对心缺血再灌注损伤心肌发挥保护作用。
关键词:远隔缺血预适应  心肌缺血/再灌注损伤  基质细胞衍生因子
The cardioprotection effects of remote ischemic preconditioning on myocardial ischemia reperfusion injury through SDF-1α/CXCR4 signal pathway    Download Fulltext
The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, 221000
Fund Project:
Abstract:
      Abstract Objective: To investigate the protective effect of remote ischemic preconditioning(PIPC) on myocardial ischemia/reperfusion(I/R) injury and underlying mechanism. Method: Clean level male white rabbits of New Zealand, weight 2.2—2.5 kg, were randomly divided into the following groups: Sham (n=6), myocardial I/R(n=6), RIPC+I/R (n=6), SDF-1α/CXCR4 inhibitor(AMD3100)+I/R, AMD3100+RIPC+I/R. The release of SDF-1α was detected by ELISA from the serum, the size of myocardial infarction was assayed by TTC, cardiomyocyte apoptosis rate was detected by TUNEL, and the expressions of Bcl-2,Bax were assessed via western blot. Result: Myocardial I/R and RIPC+I/R can promote the expressions of SDF-1α compared with Sham group(P<0.05), more obvious in RIPC+I/R group(P<0.05); Compared with I/R group, myocardium infarction area and cardiomyocyte apoptosis rate were reduced between RIPC+I/R and AMD3100+RIPC+I/R, with the increase of Bcl-2,the decrease of Bax(P<0.05). By comparing with RIPC+I/R group, myocardium infarction area and cardiomyocyte apoptosis rate were increased in AMD3100+RIPC+I/R group(P<0.05). Conclusion: RIPC can promote SDF-1α release to exert the cardioprotection effect against myocardium ischemia reperfusion injury via SDF-1α/CXCR4 signal pathway.
Keywords:remote ischemic preconditioning  ischemia/reperfusion  stromal cell derived factor-1
查看全文  查看/发表评论  下载PDF阅读器

您是本站第 12298761 位访问者

版权所有:中国康复医学会
主管单位:国家卫生和计划生育委员会 主办单位:中国康复医学会
地址:北京市朝阳区和平街北口中日友好医院内   邮政编码:100029   电话:010-64218095   

本系统由北京勤云科技发展有限公司设计 京ICP备10000329号