Protection of carbon monoxide-releasing molecule against lung injury induced by limb ischemia-reperfusion  

作　　者：周君琳 李钢 海涌 关立 黄新莉 孙鹏 

机构地区：[1]Department of Orthopedics, Beijing ChaoyangHospital, Capital Medical University, Beijing 100020, China [2]Peking North Hospital of Ministry of Ordance Industryof China, Beijing 100089, China [3]Department of Pathophysiology, Hebei MedicalUniversity, Shijiazhuang 050017,China

出　　处：《Chinese Journal of Traumatology》2009年第2期71-76,共6页中华创伤杂志（英文版）

基　　金：This project was supported by the National Natural Science Foundation of China （No. 30271337）.

摘　　要：Objective： To observe the role and mechanism of CO- releasing molecule （CORM）-2 in lung injury induced by ischemia-reperfusion （IR） of hind limbs in rats. Methods： Arat model of lung injury induced by IR of hind limbs was established. A total of 40 Sprague Dawley （SD） rats were randomly divided into 5 groups （n = 8）： sham, sham ＋ CORM-2, IR, IR ＋ CORM-2 and IR ＋ dimethyl sulfoxide （DMSO）. Rats in the IR group received hind limb ischemia for 2 hours and reperfusion for 2 hours, rats in the sham group underwent sham surgery without infrarenal aorta occlusion, rats in the IR＋CORM-2 group and in the sham ＋ CORM-2 group were given CORM-2 （10 μmol/kg intravenous bolus） 5 minutes before reperfusion or at the corresponding time points, while rats in the IR ＋ DMSO group was treated with the same dose of vehicle （DMSO） at the same time. The lung tissue structure, polymorphonuclear neutrophil （PMN） count, wet-to-dry weight ratio （W/D）, malondialdehyde （MDA） content, myeloperoxidase （MPO） activity, intercellular adhesion molecule- 1 （ICAM- 1）expression, I κBα degradation and nuclear factor （NF）-κB activity in the lungs were assessed. Results： As compared with the sham group, lung PMNs number, W/D, MDA content, MPO activity, ICAM-1 expression and NF- κB activity significantly increased in the IR group, but the level of I κBα decresed （P〈0.01）. Compared with the IR group, lung PMNs number, W/D, MDA content, MPO activity and ICAM- 1 expression significantly decreased in the IR＋COMR-2 group （P〈0.01）, while the level of IκBα increased. Conclusions： These data demonstrate that CORM-2 attenuates limb IR-induced lung injury through inhibiting ICAM-1 protein expression, NF-κB pathway and the leu- kocytes sequestration in the lungs following limb IR in rats, suggesting that CORM-2 may be used as a therapeutic agent against lung injury induced by limb IR.

关 键 词：Carbon monoxide LUNG Reperfusioninjury Nuclear factor kappa B 

分 类 号：R363[医药卫生—病理学]