Ghrelin reduces isoproterenol-induced myocardial injury and cardiomyocyte apoptosis via inhibiting endoplasmic reticulum stress

AIM:To investigate whether ghrelin (G)-reduced myocardial injury and cardiomyocyte apoptosis induced by isoproterenol (ISO) is related to the inhibition of endoplasmic reticulum stress (ERS). METHODS: Twenty-nine male Sprague Dawley (SD) rats were randomly divided into control group (n=9),ISO group (n=11) and ISO+G group (n=9). Rats in control (Con) group were subcutaneously injected with normal saline. Rats in ISO group were injected with ISO and rats in ISO+G group were injected with ghrelin 2 days before injection of ISO. Hemodynamic parameters of the rats in each group were recorded by the Power Lab system. Myocardial tissue injury was assessed by HE staining and activity determination of plasma lactate dehydrogenase (LDH) and creatinine kinase (CK)-MB. Cardiomyocyte apoptosis was detected by TUNEL method and the expression of ERS markers C/EBP-homologous protein (CHOP) and cleaved caspase-12 in myocardial tissue was detected by Western blot. RESULTS: Exogenous ghrelin alleviated heart dysfunction, reduced myocardial injury and cardiomyocyte apoptosis and inhibited overexpressions of CHOP and cleaved caspase-12. CONCLUSION: Ghrelin reduced ISO-induced myocardial injury and cardiomyocyte apoptosis via inhibiting ERS.