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 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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