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Glycine attenuates myocardial ischemia-reperfusion injury by inhibiting myocardial apoptosis in rats

机译:甘氨酸通过抑制大鼠心肌细胞凋亡来减轻心肌缺血-再灌注损伤

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摘要

Glycine is a well-documented cytoprotective agent. However, whether it has a protective effect against myocardial ischemia-reperfusion injury in vivo is still unknown. By using an open-chest anesthetized rat model, we found that glycine reduced the infarct size by 21% in ischemia-reperfusion injury rats compared with that in the vehicle-treated MI/R rats. The left ventricular ejection fraction and fractional shortening were increased by 19.11% and 30.98%, respectively, in glycine-treated rats. The plasma creatine kinase levels in ischemia-reperfusion injury rats decreased following glycine treatment. Importantly, administration of glycine significantly inhibited apoptosis in post-ischemia-reperfusion myocardium, which was accompanied by suppression of phosphorylated p38 mitogen-activated protein kinase and c-Jun NH2-terminal kinase, as well as the Fas ligand. These results suggest that glycine attenuates myocardial ischemia-reperfusion injury in vivo by inhibiting cardiomyocytes apoptosis.
机译:甘氨酸是有据可查的细胞保护剂。然而,其在体内是否对心肌缺血-再灌注损伤具有保护作用仍是未知的。通过使用开胸麻醉的大鼠模型,我们发现与载体治疗的MI / R大鼠相比,甘氨酸可将缺血再灌注损伤大鼠的梗塞面积减少21%。在甘氨酸治疗的大鼠中,左心室射血分数和缩短分数分别增加了19.11%和30.98%。甘氨酸治疗后,缺血再灌注损伤大鼠血浆肌酸激酶水平降低。重要的是,给予甘氨酸可显着抑制缺血再灌注后心肌的细胞凋亡,并伴有磷酸化p38丝裂原活化蛋白激酶和c-Jun NH2末端激酶以及Fas配体的抑制作用。这些结果表明,甘氨酸通过抑制心肌细胞的凋亡来减轻体内的心肌缺血-再灌注损伤。

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