金属硫蛋白参与肺缺血预处理的保护作用  

Involvement of metallothionein in the protection of lung ischemic preconditioning

作　　者：许冬武[1] 石璐[1,2] 贾旭广[1,2] 钱小英[3] 唐兰兰[1] 张艳华[1] 汪洋[1] 王万铁[1] 

机构地区：[1]温州医学院病理生理学教研室,温州325035 [2]桐乡市卫生学校,桐乡314500 [3]温州市第三人民医院呼吸内科,温州325000

出　　处：《生理学报》2010年第5期465-468,共4页Acta Physiologica Sinica

基　　金：supported by the Science and Technology Project of Wenzhou Municipality;Zhejiang Province;China(No.Y20060083);the Medical and Health Research Project of Wenzhou Municipality;Zhejiang Province;China(No.2009A004)

摘　　要：本实验旨在探讨金属硫蛋白是否参与肺缺血预处理(ischemic preconditioning,IP)的保护作用。实验用健康雄性Sprague-Dawley大鼠24只,随机分为对照组、肺缺血/再灌注(ischemia-reperfusion,I/R)组和IP组,对比观察各组肺组织中金属硫蛋白(metallothionein,MT)的含量,血清中丙二醛(malondialdehyde,MDA)含量、超氧化物歧化酶(superoxide dismutase,SOD)及髓过氧化物酶(myeloperoxidase,MPO)活性的变化,用原位缺口末端标记法(TUNEL)检测肺组织细胞的凋亡情况,用透射电镜观察肺组织超微结构的改变。结果显示,与对照组相比,I/R组肺组织中MT的含量显著下降(P<0.05),血清MDA含量、MPO活性明显升高(P<0.01),SOD活性明显下降(P<0.01),凋亡指数(apoptosis index,AI)显著增高(P<0.01),肺组织超微结构发生异常改变;与I/R组相比,IP组肺组织中MT的含量显著升高(P<0.01),血清MDA含量、MPO活性明显下降,SOD活性明显升高(P<0.05或P<0.01),AI为14.76±1.35,显著低于I/R组(P<0.01),肺组织超微结构显著改善。根据以上结果,我们推断诱导MT的产生可能是IP肺保护作用的机制之一。The aim of the present study was to investigate whether metallothionein was involved in the protection of lung ischemic preconditioning（IP） against lung ischemia-reperfusion（I/R） injury.Adult male Sprague-Dawley rats were randomly divided into 3 groups based upon the intervention（n=8）：control group（C）,lung I/R group（I/R）,lung I/R＋IP group（IP）.At the end of the experiment,the content of metallothionein was tested in lung tissue.Blood specimens collected from the arteria carotis were tested for the contents of malondialdehyde（MDA）,the activities of superoxide dismutase（SOD） and myeloperoxidase（MPO）.The pneumocyte apoptosis index（AI） was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling（TUNEL）.Ultrastructural changes of lung tissue were observed by using transmission electron microscope.The results showed that in I/R group,the content of metallothionein was decreased（P0.05）,the content of MDA and MPO activity were increased（P0.01）,and SOD activity was decreased（P0.01）,compared with those in control group.IP treatment significantly increased the content of metallothionein（P0.01）,attenuated the MDA level（P0.05） and MPO activity（P0.01）,and improved SOD activity（P0.01） in blood serum.The number of TUNEL-positive cells in IP group was significantly reduced compared with that in I/R group（P0.01）.There were abnormal ultrastructural changes in I/R group,which were markedly reversed in IP group.In conclusion,IP may protect lung against I/R injury by inducing the expression of metallothionein.

关 键 词：肺 缺血/再灌注损伤 缺血预处理 金属硫蛋白 

分 类 号：R363[医药卫生—病理学]