异氟醚延迟预处理对兔心肌缺血再灌注时Bcl-2和caspase-3蛋白表达的影响  

Effect of isoflurane delayed preconditioning on the expression of Bcl-2 and caspase-3 in myocardium during ischemia reperfusion in rabbits

作　　者：刘流[1] 冉珂[1] 常业恬[1] 

机构地区：[1]中南大学湘雅二医院麻醉科,长沙410011

出　　处：《中南大学学报（医学版）》2010年第4期346-350,共5页Journal of Central South University ：Medical Science

基　　金：湖南省自然科学基金(03JJY3053);湖南省科技厅资助项目(2007FJ3015)~~

摘　　要：目的:观察异氟醚延迟预处理对兔心肌缺血再灌注时Bcl-2和caspase-3蛋白表达的影响,并探讨其心肌延迟保护效应的机制。方法:40只成年雄性新西兰大白兔随机分成4组:假手术组(C组)、缺血再灌注组(I/R组)、异氟醚预处理组(S组)、异氟醚预处理+阿片类受体阻断剂组(N组)。除C组外,各组均接受左冠状动脉前降支阻断40min,再灌注120min。S组在缺血前24h时吸入2.0%异氟醚2h,N组在吸入2.0%异氟醚前10min,静脉注入阿片类受体阻断剂纳络酮6mg/kg。再灌注结束后,测心肌梗死面积,免疫印迹法测Bcl-2和caspase-3蛋白的表达,透视电镜下观察心肌超微结构变化。结果:与I/R组比,S组心梗面积(19.7%±2.8%vs37.8%±1.7%)显著降低(P<0.05),Bcl-2蛋白表达增高,caspase-3蛋白活性降低(P<0.05),心肌病理损伤减轻。结论:异氟醚预处理对心肌延迟保护效应可能与其上调Bcl-2蛋白表达和下调caspase-3蛋白活性,抑制心肌细胞凋亡有关。Objective To investigate the effect of isoflurane delayed preconditioning on the activation of caspase-3 and the expression of Bcl-2 in rabbit myocardium during ischemia reperfusion and the possible mechanism.Methods Forty New Zealand male white rabbits were randomly divided into 4 groups：a sham group （Group C）,an I/R group,an isoflurane group （Group S）,and an isoflurane ＋ opioid recepters inhibitor group （Group N）.Group S was exposed to 2.0% isoflurane for 2 h.Group N was given naloxone （6.0 mg/kg） before exposing to 2.0% isoflurane.Group C and Group I/R were exposed for 2 h to 100% oxygen,serving as untreated controls.Twenty-four hours later,Group S and Group N underwent 40 min of coronary occlusion followed by 2 h of reperfusion.At the end of the reperfusion,infarct size（IS） and area at risk（AAR） were defined by Evans and TTC staining.The myocardial ultrastructure was observed by electron microscopy.The levels of the myocardial Bcl-2 and caspase-3 expression were determined by Western blot.Results The caspase-3 activity of Group S was significantly lower than that of Group I/R（P〈0.05）.The IS was significantly reduced in Group S（19.7%±2.8%） as compared with Group I/R（37.8%±1.7%） （P〈0.05）.Microscopic examination showed less myocardial damage in Group S than in Group I/R.Conclusion Isoflurane delayed preconditioning can inhibit the apoptosis of myocardium by up-regulating the expression of Bcl-2 and down-regulating the activation of caspase-3,which may be part of the molecular mechanism of isoflurane delayed preconditioning on myocardial preservation.

关 键 词：异氟醚 延迟预处理 心肌再灌注损伤 阿片类受体 BCL-2 caspase-3 

分 类 号：R96[医药卫生—药理学]