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金属硫蛋白参与肺缺血预处理的保护作用

许冬武, 石璐, 贾旭广, 钱小英, 唐兰兰, 张艳华, 汪洋, 王万铁

温州医学院病理生理学教研室，温州 325035； 桐乡市卫生学校，桐乡 314500；温州市第三人民医院呼吸内科，温州 325000

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(superoxidedismutase, 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。

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

[Involvement of metallothionein in the protection of lung ischemic preconditioning.] [Ariticle in Chinese]

XU Dong-Wu, SHI Lu, JIA Xu-Guang, QIAN Xiao-Ying, TANG Lan-Lan, ZHANG Yan-Hua, WANG Yang, WANG Wan-Tie

Department of Pathophysiology of Wenzhou Medical College, Wenzhou 325035, China； Health School of Tongxiang, Tongxiang 314500, China； Respiration Department of the 3rd People’s Hospital of Wenzhou, Wenzhou 325000, China

Abstract

The aim of the present study was to investigate whether metallothionein was involved in the protection of lung ischemicpreconditioning (IP) against lung ischemia-reperfusion (I/R) injury. Adult male Sprague-Dawley rats were randomly divided into 3groups 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 contentsof malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and myeloperoxidase (MPO). The pneumocyte apoptosisindex (AI) was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL). Ultrastructuralchanges of lung tissue were observed by using transmission electron microscope. The results showed that in I/R group, the content ofmetallothionein was decreased (P<0.05), the content of MDA and MPO activity were increased (P<0.01), and SOD activity wasdecreased (P<0.01), compared with those in control group. IP treatment significantly increased the content of metallothionein (P<0.01),attenuated the MDA level (P<0.05) and MPO activity (P<0.01), and improved SOD activity (P<0.01) in blood serum. The number ofTUNEL-positive cells in IP group was significantly reduced compared with that in I/R group (P<0.01). There were abnormal ultrastructuralchanges in I/R group, which were markedly reversed in IP group. In conclusion, IP may protect lung against I/R injury byinducing the expression of metallothionein.

Key words: Lung; ischemia/reperfusion injury; ischemic preconditioning; metallothionein

收稿日期：2010-06-07　　录用日期：2010-09-19

通讯作者：王万铁　　E-mail: wzwwt@tom.com

引用本文：

许冬武, 石璐, 贾旭广, 钱小英, 唐兰兰, 张艳华, 汪洋, 王万铁. 金属硫蛋白参与肺缺血预处理的保护作用[J]. 生理学报 2010; 62 (5): 465-468.

XU Dong-Wu, SHI Lu, JIA Xu-Guang, QIAN Xiao-Ying, TANG Lan-Lan, ZHANG Yan-Hua, WANG Yang, WANG Wan-Tie. [Involvement of metallothionein in the protection of lung ischemic preconditioning.] [Ariticle in Chinese] . Acta Physiol Sin 2010; 62 (5): 465-468 (in Chinese with English abstract).