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

Previous Articles     Next Articles

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

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