Glycine Protects H9C2 Cardiomyocytes from High Glucose- and Hypoxia/Reoxygenation-Induced Injury via Inhibiting PKCβ2 Activation and Improving Mitochondrial Quality.

<italic>Background</italic>. Patients with diabetes are more vulnerable to myocardial ischemia reperfusion injury (IRI), which is involved in PKC<italic>β</italic>2 activation and mitochondrial dysfunction. Glycine has been documented as a cytoprotective agent to attenuate diabetes-related abnormalities and reduce myocardial IRI, but the underlying mechanisms are still unclear. We determined whether glycine could attenuate high glucose- (HG-) and hypoxia/reoxygenation- (H/R-) induced injury by inhibiting PKC<italic>β</italic>2 activation and improving mitochondrial quality in cultured H9C2 cells. <italic>Methods</italic>. H9C2 cells were either exposed to low glucose (LG) or HG conditions with or without treatment of glycine or CGP53353 (a selective inhibitor of PKC<italic>β</italic>2) for 48 h, then subjected to 4 h of hypoxia followed by 2 h of reoxygenation (H/R). Cell viability, lactate dehydrogenase (LDH) release, mitochondrial membrane potential (MMP), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) concentration were detected using corresponding commercial kits. Mitochondrial quality control-related proteins (LC-3II, Mfn-2, and Cyt-C) and PKC<italic>β</italic>2 activation were detected by Western blot. <italic>Results</italic>. HG stimulation significantly decreased cell viability and SOD activity and increased LDH release, MDA production, and PKC<italic>β</italic>2 activation as compared to LG group, all of which changes were further increased by H/R insult. Glycine or CGP53353 treatment significantly reduced the increase of LDH release, MDA production, PKC<italic>β</italic>2 activation, and Cyt-C expression and the decrease of cell viability, SOD activity, MMP, Mfn-2 expression, and LC-3II/LC-3I ratio induced by HG and H/R stimulation. <italic>Conclusions</italic>. Supplementary glycine protects H9C2 cells from HG- and H/R-induced cellular injury by suppressing PKC<italic>β</italic>2 activation and improving mitochondria quality. [ABSTRACT FROM AUTHOR]