Abstract
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.
Highlights
Myocardial infarction (MI) is an important contributor to cardiovascular mortality
To investigate the effect of glycine on myocardial I/R injury in vivo, we used Sprague-Dawley rats subjected to 30 min of myocardial ischemia followed by 6 h of reperfusion as an experimental model
When rats were pretreated with glycine, the ischemic area in the area at risk was significantly decreased by 21.74% (34.58%±1.22% in the vehicle group vs 27.06%±1.73% in the glycine treatment group, n = 6) after myocardial I/R
Summary
Myocardial infarction (MI) is an important contributor to cardiovascular mortality. Reperfusion is considered as a double-edged sword as it can lead to worsening of tissue injury[1]. *Corresponding author: Xiaoyu Li, M.D., Ph.D, Atherosclerosis Research Center, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu cludes distinct phases of cellular injury with adenosine triphosphate (ATP) depletion, lactate accumulation and acidosis observed during ischemia, and the production of reactive oxygen and nitrogen species during reperfusion[2]. Myocardial protection against I/R injury becomes a primary goal of therapeutic intervention. A non-essential amino acid, protects mammalian cells against ischemic cell injury by preventing cellular membrane leakage. Glycine offers protection against I/R injury in vivo in the kidney[3], liver[4,5,6], 210029, China.
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