Key result
Pre-ischemia diosgenin lowers CK and MDA and boosts antioxidants via mitochondrial ATP-sensitive K+ channels.
Why the study?
The role of mitochondrial ATP-sensitive K+ channels in mediating the antioxidative effects of diosgenin on myocardial ischemia-reperfusion injury was investigated.
Does diosgenin reduce oxidative stress and myocardial injury in rat hearts subjected to ischemia-reperfusion?
Does diosgenin reduce oxidative stress and myocardial injury in rat hearts subjected to ischemia-reperfusion?
p-value: p=<0.05
Diosgenin exerts cardioprotective effects against ischemia-reperfusion injury in rat hearts by attenuating oxidative stress, likely mediated through the opening of mitochondrial ATP-sensitive K+ channels.
Diosgenin pretreatment reduced oxidative markers in rat I/R hearts; leaves open whether effects translate to human cardioprotection.
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.
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Badalzadeh et al. (2015) studied Myocardial ischemia-reperfusion injury (n=30). Diosgenin vs. Control (normal K-H solution) and Cremophor-EL was evaluated on Creatine kinase (CK) and malondialdehyde (MDA) levels (p=<0.05). Diosgenin administration before ischemia significantly lowered creatine kinase and malondialdehyde levels (p < 0.05) and increased antioxidant enzyme activities, effects that were reversed by blocking mitochondrial ATP-sensitive K+ channels.
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