失血性休克缺血-再灌注损伤家兔肺泡巨噬细胞中IκK-β/NF-κB改变的实验研究  

Experimental study on the changes of IκK-β/NF-κB in alveolar macrophagesin the process of ischemia-reperfusion injury following hemorrhagic shock

作　　者：尹文[1] 童卫[2] 熊利泽[3] 刘健[1] 黄杨[1] 虎晓岷[1] 裴建明[4] 张金山[4] 

机构地区：[1]第四军医大学西京医院急诊科,陕西西安710032 [2]第四军医大学西京医院医教部,陕西西安710032 [3]第四军医大学西京医院麻醉科,陕西西安710032 [4]第四军医大学基础部,陕西西安710032

出　　处：《创伤外科杂志》2008年第1期54-56,共3页Journal of Traumatic Surgery

基　　金：军队"十一五"医药卫生科研基金项目(06AM226);军队"科技攻关"医药卫生科研基金项目(06G086)

摘　　要：目的观察失血性休克缺血-再灌注(I/R)损伤时兔肺泡巨噬细胞(AM)中I-κB激酶-β/核因子-κB(IκK-β/NF-κB)信号通路的改变,探讨肺部炎症损伤的细胞分子基础。方法建立失血性休克I/R家兔模型,分离、培养AM,用原位杂交方法检测AM中IκK-β的mRNA表达,用凝胶电泳迁移率改变分析法(EMSA)和酶联免疫吸附(ELISA)法分别检测AM中NF-κB的活性和AM培养上清液中TNF-α、IL-6的含量。病理学光镜观察肺组织的炎症损害。结果模型组IκK-β、NF-κB、TNF-α、IL-6指标较对照组显著升高(P<0.01);I/R损伤动物肺组织呈现明显炎症病理改变。结论AM是I/R损伤炎症信号通路的重要细胞基础;细胞内IκK-β激活/NF-κB核移位/细胞因子产生是I/R肺组织炎症病理损伤的重要分子机制。Objective To study the molecular changes of IκK-β/NF-κB pathway in alveolar macrophages （AMs） in the process of I/R and explore the possible mechanism of inflammatory lung injury. Methods The rab- bit model of I/R was established, AMs were separated and cultured. Hybridization was applied to explore IκK- βmRNA expression in AMs;EMSA was used to detect NF-κB translocation and ELISA was used to detect levels of TNF-α and IL-6 in the supernatant of cell cultures. Finally,inflammatory injury in the lung was studied under microscope. Results The index of IκK-β, NF-κB,TNF-α,IL-6 in the model group increased significantly comparing with that in the control group. More severe inflammatory changes presented in the lung tissues of models of I/R than that in the control group. Conclusion AMs are the major sensitive cells in the changes of NF-κB signal pathway and plays critical role in the inflammatory injury. IkappaB kinase（IκK） activation contributes to NF-κB translocation,thus leads to the release of multiple cytokines and finally causes inflammatory injury in the lung tissue.

关 键 词：缺血-再灌注 肺泡 巨噬细胞 I-κB激酶 核因子-ΚB 失血性休克 

分 类 号：R605.971.02[医药卫生—急诊医学]