Mitochondrial ATP-sensitive K+ channels mediate the antioxidative influence of diosgenin on myocardial reperfusion injury in rat hearts

Abstract

The contribution of reactive oxygen species and oxidative stress in the pathogenesis of ischemia-reperfusion (I/R) injury has been supported by many studies. The effect of diosgenin on oxidative stress induced by I/R injury was evaluated in this study. Rat hearts were subjected to 30 minutes of global ischemia followed by 90 minutes of reperfusion. 5-hydroxydecanoate (5-HD) was used before administration of diosgenin and before ischemia. The activities of myocardial creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were measured. Administration of diosgenin before ischemia significantly lowered CK and MDA levels as compared with control group (p < 0.05) and increased GPX (p < 0.05) and SOD (p < 0.01) activities in comparison with control group. Pre-administration of 5-HD significantly attenuated the protective effects of diosgenin. In conclusion, opening of mitochondrial ATP-sensitive K+ channels and attenuating of oxidative stress can be suggested as underlying mechanisms for cardioprotective effect of diosgenin in I/R injury.