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

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。

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

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.