Journal of Biomedical Research · 2012 · 35 citations · 32 references
MedicineCardiologyPharmacologyApoptosisCellular PharmacologyPharmacodynamicsCardiovascular Molecular PhysiologyIschemic Heart DiseaseNeuroprotectionC-jun N-terminal Kinase SignalingFas LigandFas Ligand-mediated ApoptosisInfarct Size AssessmentJun N-terminal Kinase SignalingMechanisms Of Cardiac InjuryMyocardial Ischemia-reperfusion InjuryP38 Mitogen-activated Protein Kinase Signaling
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.
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Lars E. French, Michael Hahne, I. Viard et al. · The Journal of Cell Biology · 1996 · 458 citations · Full text
The β Subunit Determines the Ligand Binding Properties of Synaptic Glycine Receptors
Joanna Grudzinska, Rudolf Schemm, Svenja Haeger et al. · Neuron · 2005 · 357 citations · Full text