小鼠烟雾吸入伤后肺组织中IKK/NF-κB表达的变化及意义

The Changes and Its Significances of IKK/NF-κ B of Lung Tissue in Mice after Smoke Inhalation Injury

目的:探讨IKK/NF-kB调控的炎症反应在小鼠烟雾吸入伤后早期肺组织损伤中的作用。方法:建立小鼠烟雾吸入伤模型,将60只C57BL/6小鼠随机分成正常对照组,烟雾吸入性损伤后2 h、8 h和24 h组,观察肺组织病理改变,免疫组织化学测定肺组织NF-kBp65,IKK1和IKK2的表达,酶联免疫吸附法(ELISA)测定肺组织TNF-α,IL-6和IL-1β含量。结果:病理切片显示正常对照组小鼠肺组织无明显异常,烟雾吸入后2 h,8 h,24 h组肺部出现不同程度的炎细胞浸润、出血、水肿等;伤后2 h组、8 h组、24 h组肺组织NF-κB p65、IKK1、IKK2免疫组化评分均高于正常组小鼠(P<0.05);肺组织TNFα、IL-6和IL-1β含量在烟雾吸入后2h、8h、24h均高于正常对照组(P<0.05)。结论:NF-κB信号通路与烟雾吸入伤早期肺内大量炎症因子的释放密切相关,可能是导致伤后肺组织病理性损伤的重要因素。

Objective： To investigate the effect of inflammation-mediated by IKK/NF-K B on lung tissue of mice at early stage after smoke inhalation injury. Methods： The model of smoke inhalation injury in mice was set up. Sixty C57BL/6 mice were randomly divided into four groups-control group, and the groups of 2 h, 8 h and 24 h following smoke inhalation. The lung tissues from each group were collected to observe the pathological alteration, evaluate histological scores of NF-KB p65,IKKland IKK2 with immunohistochemistry stain, and to measure the concentration of TNF-α, IL- 6 and IL-1β with enzyme- linked immunosorbent assay （ELISA）. Results： The pathological analysis showed that there was the normal structure and no inflammatory reaction in the lungs of the control group mice, but in the 2h, 8h and 24h group after smoke inhalation injury inflammatory cells infiltration, hemorrhage, and alveolar wall edema emerged at different levels. Histological scores ofNF-KBp65, IKK1 and IKK2 were higher in the 2h, 8h and 24h group than that in the normal mice group （P〈0.05）. The concentration ofTNF-e~, IL- 6 and IL-l[3 were higher in the 2 h, 8 h and 24 h group compared with that in the normal mice group（P〈0.05）. Conclusions： The signal pathway mediated by NF-K B may be bound up with the release of massy inflammatory cy- tokines after smoke inhalation injury, and may be one of the main factors that cause the seriously pathological injury of lungs in the mice.