CAJ | 학술논문

目的：评价蛋白激酶C （PKC ）在缺血预处理减轻大鼠心肌缺血再灌注时线粒体损伤中的作用。方法雄性SD大鼠40只，12～13周龄，体重280～320 g ，采用随机数字表法，将其分为4组（ n＝10）：假手术组（S组）、缺血再灌注组（I/R组）、缺血预处理组（IPC组）和PKC抑制剂白屈菜红碱组（C组）。采用结扎左冠状动脉前降支35 min ，再灌注120 min的方法建立心肌缺血再灌注损伤模型。IPC组于缺血前即刻缺血5 min ，再灌注5 min ，重复3次，行缺血预处理。C组于缺血预处理前尾静脉注射PKC抑制剂白屈菜红碱1 mg/kg。再灌注120 min时处死大鼠取心肌组织，分离线粒体，制备线粒体悬液，测定琥珀酸脱氢酶（SDH）、黄嘌呤氧化酶（XOD ）、谷胱甘肽过氧化物酶（GSH-Px ）和Ca2＋-ATP酶的活性、Ca2＋含量、线粒体通透性转换孔（mPTP ）开放程度和膜电位（Δψm ）。结果与S组比较，I/R组线粒体XOD、Ca2＋-ATP酶活性、Ca2＋含量、mPTP开放度升高，线粒体SDH、GSH-Px的活性、Δψm降低（ P＜0.05）；与I/R组比较，IPC组线粒体XOD、Ca2＋-ATP酶活性、Ca2＋含量和mPTP开放度降低，SDH、GSH-Px的活性、线粒体Δψm升高（ P＜0.05）；与IPC组比较，C组线粒体XOD、Ca2＋-ATP酶活性、Ca2＋含量和mPTP开放度升高，线粒体SDH、GSH-Px的活性、Δψm降低（ P＜0.05）。结论 PKC参与了缺血预处理减轻大鼠心肌缺血再灌注时的线粒体损伤。
목적：평개단백격매C （PKC ）재결혈예처리감경대서심기결혈재관주시선립체손상중적작용。방법웅성SD대서40지，12～13주령，체중280～320 g ，채용수궤수자표법，장기분위4조（ n＝10）：가수술조（S조）、결혈재관주조（I/R조）、결혈예처리조（IPC조）화PKC억제제백굴채홍감조（C조）。채용결찰좌관상동맥전강지35 min ，재관주120 min적방법건립심기결혈재관주손상모형。IPC조우결혈전즉각결혈5 min ，재관주5 min ，중복3차，행결혈예처리。C조우결혈예처리전미정맥주사PKC억제제백굴채홍감1 mg/kg。재관주120 min시처사대서취심기조직，분리선립체，제비선립체현액，측정호박산탈경매（SDH）、황표령양화매（XOD ）、곡광감태과양화물매（GSH-Px ）화Ca2＋-ATP매적활성、Ca2＋함량、선립체통투성전환공（mPTP ）개방정도화막전위（Δψm ）。결과여S조비교，I/R조선립체XOD、Ca2＋-ATP매활성、Ca2＋함량、mPTP개방도승고，선립체SDH、GSH-Px적활성、Δψm강저（ P＜0.05）；여I/R조비교，IPC조선립체XOD、Ca2＋-ATP매활성、Ca2＋함량화mPTP개방도강저，SDH、GSH-Px적활성、선립체Δψm승고（ P＜0.05）；여IPC조비교，C조선립체XOD、Ca2＋-ATP매활성、Ca2＋함량화mPTP개방도승고，선립체SDH、GSH-Px적활성、Δψm강저（ P＜0.05）。결론 PKC삼여료결혈예처리감경대서심기결혈재관주시적선립체손상。
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 .