Apelin protects against cardiomyocyte apoptosis induced by glucose deprivation.

摘要: BACKGROUND Apoptosis is a major cause of ischemic heart dysfunction. Apelin, the endogenous ligand for G-protein-coupled APJ receptor, has been reported to exert cardioprotective effects during myocardial injury. The aim this study was investigate apelin on apoptosis rat cardiomyocytes induced by glucose deprivation (GD) and related signaling pathway. METHODS Apelin mRNA expression were determined RT-PCR in neonatal different durations GD. Cardiomyocyte detected annexin V-FITC/propidium iodide (PI) staining after GD 12 hours with or without apelin-13 (10 100 nmol/L) pretreatment. Protein levels Akt mammalian target rapamycin (mTOR) as well cell presence absence LY294002 (a phosphatidylinositol 3-kinases (PI3K) inhibitor) mTOR inhibitor). RESULTS up-regulated when exposed 6, 12, 18, 24 compared base level (P > 0.05, P < 0.01, 0.01). However, up 36 hours, 17% lower than 0.05). paralleled that apelin. Apelin-13 pretreatment at nmol/L significantly inhibited GD-induced cardiomyocyte 0.05) increased phosphorylation At same time (100 Bcl-2 protein down-regulated Bax cleaved caspase-3 anti-apoptotic effect blocked 0.01) but not rapamycin. CONCLUSIONS apelin-APJ system compensatorily ultimately following sustained ischemia. protects against via activation PI3K/Akt