Abstract
Objective To evaluate the role of protein kinase C （PKC ） in reduction of mitochondrial injury during myocardial ischemia-reperfusion （I/R） by ischemic preconditioning in rats .Methods Forty male Sprague-Dawley rats ,aged 12-13 weeks ,weighing 280-320 g ,were randomly divided into 4 groups （ n=10 each） using a random number table：sham operation group （S group） ,I/R group ,ischemic preconditioning group （IP group） and PKC inhibitor chelerythrine group （C group） .Myocardial I/R was produced by 35 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion .Ischemic preconditioning was induced by 3 episodes of 5 min occlusion of left anterior descending branch at 5 min intervals before myocardial ischemia . Chelerythrine 1 mg/kg was injected intravenously via the caudal vein before ischemic preconditioning in group C . At 120 min of reperfusion ,the animals were sacrificed and the hearts were immediately removed .Mitochondrial suspension was prepared for determination of activities of succinate dehydrogenase （SDH ） , xanthine oxidase （XOD ） , glutathione peroxidase （GSH-Px ） and Ca2＋-ATPase , content of Ca2＋ , myocardial mitochonerial permeability transition pore （mPTP） opening and membrane potential （Δψm ） .Results Compared with S group , the activities of XOD and Ca2＋-ATPase ,content of Ca2＋ and mPTP opening were significantly increased ,and the＆nbsp;activities of SDH and GSH-Px and Δψm were decreased in I/R group （ P〈0.05） .Compared with I/R group ,the activities of XOD and Ca2＋-ATPase , content of Ca2＋ and mPTP opening were significantly decreased , and the activities of SDH and GSH-Px and Δψm were increased in IP group （ P〈0.05） .Compared with IP group ,the activities of XOD and Ca2＋-ATPase , content of Ca2＋ and mPTP opening were significantly increased , and the activities of SDH and GSH-Px and Δψm were decreased in C group （ P〈0.05） .Conclusion PKC is involved in reduction of mitochondrial injury during myocardial I/R by ischemic preconditioning in rats . Key words: Protein kinase C; Ischemic preconditioning; Myocardial reperfusion injury; Mitochondria
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