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Late anti‐apoptotic effect of KATP channel opening in skeletal muscle

Necrosis and apoptosis caused by ischaemia–reperfusion (IR) result in myocyte death and atrophy. ATP‐sensitive K+ (KATP) channels activation increases tissue tolerance of IR‐injury. Thus, in the present study, we evaluated the effects of KATP channel activation on skeletal muscle apoptosis after IR. Male Wistar rats were treated with 40 mg/kg, i.p., diazoxide (a KATP channel opener) or 5 mg/kg, i.p., glibenclamide (a KATP channel inhibitor) 30 min before the induction of 3 h ischaemia, followed by 6, 24 or 48 h reperfusion. At the end of the reperfusion period, the gastrocnemius muscle was removed for the analysis of tissue malondialdehyde content, superoxide dismutase (SOD) and catalase (CAT) activity, Bax and Bcl‐2 protein expression, histological damage and the number of apoptotic nuclei. Ischaemia–reperfusion increased malondialdehyde content (P < 0.01) and Bax expression (P < 0.01) and induced severe histological damage, in addition to decreasing CAT and SOD activity (P < 0.01 and P < 0.05, respectively) and Bcl‐2 expression (P < 0.01). Diazoxide reversed the effects of IR on tissue damage, MDA content, SOD and CAT activity (after 6 and 24 h reperfusion; P < 0.05) and Bax and Bcl‐2 expression (after 24 and 48 h reperfusion; P < 0.01). In contrast, glibenclamide pretreatment had no effect. The number of apoptotic nuclei in the IR and glibenclamide‐pretreated groups increased significantly (P < 0.001 vs Sham). In contrast, diazoxide pretreatment decreased the number of apoptotic nuclei compared with the IR group (P < 0.01). The results of the present study suggest that the KATP channel activator diazoxide attenuates lipid peroxidation during the first hour of reperfusion and modulates apoptotic pathways at later time points.