| Objective—The growth hormone (GH)-releasing peptide ghrelin exerts a cardio-protective effect independent of GH release. However, the cellular and molecular mechanisms underlying ghrelin cardioprotective activity are not known. In the present study, the effects of ghrelin on the hypoxia/reoxygenation injury of endothelial cells were evaluated.Methods—Human umbilical vein endothelial cells(ECV304) were incubated in vitro with or without human ghrelin (1×10-8M,1×10-7M,1×10-6M) . The cells were exposed to hypoxia for 6 hours and subsquently reoxygenated for half an hour. The survival ratio of endothelial cells were calculated. Lactic dehydrogenase(LDH), nitric oxide(NO), nitric oxide synthase (NOS) and the expression of NF-kB in the nucleus were examined.Results—Ghrelin significantly increases the survival ratio (83.27% vs 92.13%) of endothelial cells exposed to hypoxia/reoxygenation injury, upregulates the production of eNOS and NO (23.76umol/L vs 51.62umol/L), inhibits the activation of NF-kB in the nucleus, decreases the formation of MDA and LDH release (164.21U/L vs 16.47U/L) (P<0.05). It also slightly downregulates the production of iNOS induced by long-time hypoxia.Conclusions—Ghrelin protects endothelial cells against hypoxia/reoxygenation injury at least partially as a result of the increased production of NO and inhibition of NF-kB.
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