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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。
OBJECTIVE: To establish an animal model of myocardial ischemia / reperfusion (I / R) and investigate the effect of sRAGE on cardiac function and cardiomyocyte apoptosis induced by ischemia-reperfusion. Methods C57BL / 6J mice model of cardiac ischemia-reperfusion was established. The cardiac function was detected by ultrasound. The degree of cardiomyocyte apoptosis was evaluated by TUNEL staining and Caspase-3 activity assay. Results Compared with sham group, left ventricular ejection fraction decreased in I / R group (72.4 ± 2.1% in sham group, 30.9 ± 3.2% in I / R group, P <0.05] The number of TUNEL-positive cardiomyocytes in sham group was (40.7 ± 1.6)%, while in I / R group was (15.1 ± 2.0)%, P <0.05] 20.0 ± 1.6%, P <0.05]. The activity of Caspase-3 was increased in the Sham group (1.00 ± 0.2)% compared with the I / R group (2.64 ± 0.4)%, P <0.05. Compared with the I / R group, sRAGE pretreatment significantly increased the left ventricular ejection fraction [(46.5 ± 2.0)% P <0.05] and short axis shortening [(23.0 ± 1.1)%, P <0.05] While decreasing the number of TUNEL positive cardiomyocytes [(9.2% ± 1.0)% P <0.05], and Caspase-3 activity [(1.94% ± 0.1)% P <0.05]. Conclusion sRAGE can significantly reduce the cardiac function induced by ischemia-reperfusion and inhibit cardiomyocyte apoptosis.