Abstract: AIM: To investigate the protective effects of Diazoxide, a selective mitoKATP opener, on the cardiac myocytes damages induced by oxidative stress and to discuss its mechanism.METHODS: Oxidative damage cell model was induced by hydrogen peroxide (H2O2 500 μmol·L^-1).Lactate dehydrogenase (LDH) activities in the medium and mitochondrial membrane potential assessed in flow cytometry by dual labelling with rhodamine-123 (Rh-123) and propidium were measured in the diazoxide(100 μmol·L^-1 ) pretreated and un-pretreated groups.RESULTS: The level of LDH and the percentage of injured cells in H2O2 exposure group after 2 h injury were significantly higher than those in the control group(P<0.01).On the contrary, after exposure to H2O2 ,the Rh-123 fluorescence intensity was significantly decreased.Compared with simple injury group, pre-treatmentwith diazoxide (100 μmol·L^-1 ) could obviously attenuateH2O2 induced cytotoxicity, which could be abrogated by the mitoKATP channel blocker 5-hydroxydecanoate(500 μmol·L^-1).CONCLUSION: Diazoxide exerts significant protective effects against the damages induced by H2O2 in the cultured neonatal rat cardiomyocytes,which may be mediated by activation of mitoKATP channels.

Key words: diazoxide, mitoKATP channels, myocardial cell, oxidative stress