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J Biomed Res. 2012 Sep;26(5):346-54. doi: 10.7555/JBR.26.20110124. Epub 2012 Jun 29.

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

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Atherosclerosis Research Center, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China;


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.


apoptosis; cardiomyocytes; glycine; glycine receptor α2 subunit; ischemia reperfusion

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