| Aim: Nicorandil has been reported to induce the cardioprotection by opening the mitochondrial KATP channels of the myocardiocytes. Up to now the mechanism of cardioprotection is not fully understood. The purpose of present study was to investigate the cardioprotective effect of nicorandil on the heart ischemia-reperfusion the rats.Methods: 50 rats were randomly divided into 5 groups as follows: Group A: control group Group. B: ischemia-reperfusion group. Group C: nicorandil (5mg/kg) was administrated by intravenous injection at 15 minutes before the artery occlusion. Group D: nicorandil (5mg/kg) was administrated at the onset of the reperfusion. Group E: nicorandil (5mg/kg) was administrated intravenous injection at 15 minutes after the artery occlusion. After the reperfusion, the serum lactate dehydrogenase (LDH) activity, the total superoxide dismutase (SOD) activity and the malondialdehyde (MDA) content of myocardial tissue were measured. The myocardial ultrastructure was observed with electron microscope. The expression of the anti-apoptotic protein Bcl-2 and the apoptotic protein Bax were detected by immunohistochemical staining. The mitochondrial membrane potential was detected by spectrophotometer.Results: The results of the nicorandil groups (group C, D, E) were compared with that of group B, the activity of LDH and the level of MDA decreased and the activity of SOD increased in nicorandil group (P<0.01, P<0.05). The positive staining level of the expressed Bcl-2 was increased, the positive staining level of the expressed Bax was decreased (P<0.01). The mitochondrial membrane potential was increased in the nicorandil groups compared with that of group B (P<0.05). Conclusion: Nicorandil can have a cardioprotective function on the heart with the ischemia-reperfusion in the rats. The cadioprotective effect of nicorandil may be based on the opening of the mitochondrial KATP channel. |
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