Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats  

作　　者：Jie CUI Zhi LI Ling-bo QIAN Qin GAO Jue WANG Meng XUE Xiao-e LOU Iain C.BRUCE Qiang XIA Hui-ping WANG 

机构地区：[1]Department of Physiology,School of Medicine,Zhejiang University [2]Department of Physiology,Xuzhou Medical College [3]Department of Physiology,Zhejiang Medical College

出　　处：《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》2013年第6期487-495,共9页浙江大学学报（英文版）B辑（生物医学与生物技术）

基　　金：Project (Nos. 2011C23105 and 2012C33088) supported by the Department of Science and Technology of Zhejiang Province,China

摘　　要：Objective:To investigate the beneficial effect of bicyclol on rat hearts subjected to ischemia-reperfusion(IR) injuries and its possible mechanism.Methods:Male Sprague-Dawley rats were intragastrically administered with bicyclol(25,50 or 100 mg/(kg·d)) for 3 d.Myocardial IR was produced by occlusion of the coronary artery for 1 h and reperfusion for 3 h.Left ventricular hemodynamics was continuously monitored.At the end of reperfusion,myocardial infarct was measured by 2,3,5-triphenyltetrazolium chloride(TTC) staining,and serum lactate dehydrogenase(LDH) level and myocardial superoxide dismutase(SOD) activity were determined by spectrophotometry.Isolated ventricular myocytes from adult rats were exposed to 60 min anoxia and 30 min reoxygenation to simulate IR injuries.After reperfusion,cell viability was determined with trypan blue;reactive oxygen species(ROS) and mitochondrial membrane potential of the cardiomyocytes were measured with the fluorescent probe.The mitochondrial permeability transition pore(mPTP) opening induced by Ca2+(200 μmol/L) was measured with the absorbance at 520 nm in the isolated myocardial mitochondria.Results:Low dose of bicyclol(25 mg/(kg·d)) had no significant improving effect on all cardiac parameters,whereas pretreatment with high bicyclol markedly reduced the myocardial infarct and improved the left ventricular contractility in the myocardium exposed to IR(P<0.05).Medium dose of bicyclol(50 mg/(kg·d)) markedly improved the myocardial contractility,left ventricular myocyte viability,and SOD activity,as well decreased infarct size,serum LDH level,ROS production,and mitochondrial membrane potential in rat myocardium exposed to IR.The reduction of ventricular myocyte viability in IR group was inhibited by pretreatment with 50 and 100 mg/(kg·d) bicyclol(P<0.05 vs.IR),but not by 25 mg/(kg·d) bicyclol.The opening of mPTP evoked by Ca2+ was significantly inhibited by medium bicyclol.Conclusions:Bicyclol exerts cardioprotection against IR injury,at least,via reducing oxidative stress aObjective：To investigate the beneficial effect of bicyclol on rat hearts subjected to ischemia-reperfusion（IR） injuries and its possible mechanism.Methods：Male Sprague-Dawley rats were intragastrically administered with bicyclol（25,50 or 100 mg/（kg·d）） for 3 d.Myocardial IR was produced by occlusion of the coronary artery for 1 h and reperfusion for 3 h.Left ventricular hemodynamics was continuously monitored.At the end of reperfusion,myocardial infarct was measured by 2,3,5-triphenyltetrazolium chloride（TTC） staining,and serum lactate dehydrogenase（LDH） level and myocardial superoxide dismutase（SOD） activity were determined by spectrophotometry.Isolated ventricular myocytes from adult rats were exposed to 60 min anoxia and 30 min reoxygenation to simulate IR injuries.After reperfusion,cell viability was determined with trypan blue;reactive oxygen species（ROS） and mitochondrial membrane potential of the cardiomyocytes were measured with the fluorescent probe.The mitochondrial permeability transition pore（mPTP） opening induced by Ca2＋（200 μmol/L） was measured with the absorbance at 520 nm in the isolated myocardial mitochondria.Results：Low dose of bicyclol（25 mg/（kg·d）） had no significant improving effect on all cardiac parameters,whereas pretreatment with high bicyclol markedly reduced the myocardial infarct and improved the left ventricular contractility in the myocardium exposed to IR（P〈0.05）.Medium dose of bicyclol（50 mg/（kg·d）） markedly improved the myocardial contractility,left ventricular myocyte viability,and SOD activity,as well decreased infarct size,serum LDH level,ROS production,and mitochondrial membrane potential in rat myocardium exposed to IR.The reduction of ventricular myocyte viability in IR group was inhibited by pretreatment with 50 and 100 mg/（kg·d） bicyclol（P〈0.05 vs.IR）,but not by 25 mg/（kg·d） bicyclol.The opening of mPTP evoked by Ca2＋ was significantly inhibited by medium bicyclol.Conclusions：Bicyclo

关 键 词：Ischemia-reperfusion injury CARDIOPROTECTION Oxidative stress Mitochondrial permeability transition pore BICYCLOL 

分 类 号：R54[医药卫生—心血管疾病]