解剖学报

解剖学报 ›› 2015, Vol. 46 ›› Issue (2): 202-207.doi: 10.16098/j.issn.0529-1356.2015.02.010

• 细胞和分子生物学 • 上一篇    下一篇

可溶性糖基化终末产物受体抑制动物缺血再灌注导致的心功能障碍及心肌细胞凋亡

郭彩霞1* 江雪1 曾翔俊2 王红霞2 杜凤和1 陈步星1*   

  1. 1.首都医科大学附属北京天坛医院心内科，北京 100050; 2.首都医科大学基础医学院病理生理学教研室，北京 100069
  • 收稿日期:2014-09-28 修回日期:2014-12-01 出版日期:2015-04-06 发布日期:2015-04-06
  • 通讯作者: 郭彩霞;陈步星 E-mail:ttxnkx@163.com
  • 基金资助:

    国家自然科学基金资助项目;北京市科技新星计划资助项目;北京市卫生系统高层次卫生技术人才资助项目

Soluble form of the receptor for advanced glycation end products inhibits cardiac dysfunction and myocardial apoptosis induced by ischemia-reperfusion

GUO Cai-xia 1* JIANG Xue1 ZENG Xiang-jun2 WANG Hong-xia2 DU Feng-he1 CHEN Bu-xing 1*   

  1. 1.Department of Cardiology, Beijing Tiantan Hospital, Capital Medical University，Beijing 100050,China; 2.Department of Pathophysiology, School of Basic Medical Science, Capital Medical University，Beijing 100069,China
  • Received:2014-09-28 Revised:2014-12-01 Online:2015-04-06 Published:2015-04-06
  • Contact: GUO Cai-xia; CHEN Bu-xing E-mail:ttxnkx@163.com

摘要：

目的 建立动物心脏缺血再灌注模型，探讨可溶性糖基化终末产物受体（sRAGE）对缺血再灌注诱导的心功能及心肌细胞凋亡的作用。 方法 复制C57BL/6J小鼠心脏缺血再灌注模型，利用超声检测心功能；通过TUNEL染色及Caspase-3活性检测，评价心肌细胞凋亡的程度。 结果 与sham组比较，I/R组左室射血分数降低［sham组为（72.4±2.1）%，I/R组为（30.9±3.2）%，P<0.05］，短轴缩短率降低［sham组为(40.7±1.6)%, I/R组为（15.1±2.0）% , P<0.05］，TUNEL阳性心肌细胞数目增加［sham组为(1.0±0.2)%, I/R组为（20.0±1.6）% , P<0.05］, Caspase-3活性升高［（sham组(1.00±0.2）%比I/R组（2.64±0.4）%，P<0.05）。与I/R组相比较，sRAGE预处理能够明显升高左室射血分数［（46.5±2.0）% P<0.05］,增加短轴缩短率［（23.0±1.1）%，P<0.05］,同时降低TUNEL阳性心肌细胞数目［（9.2%±1.0）% P<0.05］,和Caspase-3活性［（1.94%±0.1）% P<0.05］。 结论 sRAGE能够明显改善缺血再灌注诱导的心功能降低，并抑制心肌细胞的凋亡。

关键词: 可溶性糖基化终末产物受体, 缺血再灌注, 心功能, 心肌细胞, 原位缺口末端标记, 小鼠

Abstract:

Objective To test the effect of sRAGE on cardiac function and myocardial apoptosis induced by ischemia-reperfusion in vivo. Methods C57BL/6J mice with the ligation of left anterior descending coronary artery were used as the in vivomodel. At the end of reperfusion, cardiac function was evaluated with echocardiography, and myocardial apoptosis was detected by TUNEL staining and caspase-3 activaty. Results Compared to the sham group, I/R decreased left ventricular ejection fractions (EF)［(30.9±3.2)% vs (72.4±2.1)%，P<0.05］, and left ventricular fractional shortening (FS)［(15.1±2.0)% vs( 40.7±1.6)%, P<0.05］, and then increased TUNEL ［(20.0±1.6)% vs(1.0±0.2)%,P<0.05］, and Caspase-3 activaty ［(2.64±0.4)% vs(1.00±0.2)%, P<0.05］. Compared to I/R group, sRAGE pretreatment significantly improved EF ［(46.5±2.0)% vs (30.9±3.2)%, P<0.05］, and FS［ (23.0±1.1)%vs (15.1±2.0)%, P<0.05］, decreased TUNEL ［(9.2±1.0)% vs (20.0±1.6)%,P<0.05］, and Caspase-3 activaty［ (1.94±0.1)% vs (2.64±0.4)% ,P<0.05］. Conclusion sRAGE inhibits cardiac dysfunction and myocardial apoptosis induced by ischemia-reperfusion in vivo.

Key words: Soluble form of receptor for advanced glycation end product, Ischemia-reperfusion, Cardiac function, Myocardium, Terminal UTP nick end labeling, Mouse