Skeletal muscle post-conditioning by diazoxide, anti-oxidative and anti-apoptotic mechanisms

摘要: Pretreatment with diazoxide, K(ATP) channel opener, increases tissue tolerance against ischemia reperfusion (IR) injury. In clinical settings pretreatment is rarely an option therefore we evaluated the effect of post-ischemic treatment diazoxide on skeletal muscle IR Rats were treated either saline, (K(ATP) opener; 40 mg/kg) or 5-hydroxydecanoate (5-HD; mitochondrial inhibitor; after (3 h) and (6, 24 48 h). Tissue contents malondialdehyde (MDA), superoxide dismutase (SOD) catalase (CAT) activities, Bax Bcl-2 protein expression histology determined. Apoptosis was examined (24 ischemia. induced severe histological damage, increased MDA content h; p < 0.01) decreased CAT SOD activities (6 h, 0.01 0.05), no significant expression. Diazoxide reversed effects 0.05 h damage. also 0.05) 0.01). Post-ischemic 5-HD had Number apoptotic nuclei in groups significantly (p 0.001) while apoptosis The results suggested that decrease oxidative stress acute phase which modulates proteins late Involvement KATP channels this require further evaluations.