NF-κB活化在烟雾吸入性损伤发生中的作用及地塞米松对其影响

THE ROLE OF NF-κB ACTIVATION IN THE PATHOGENESIS OF SMOKE INHALATION INJURY AND THE EFFECTS OF DEXAMETHASONE ON IT

为探讨NF κB活化在大鼠烟雾吸入性损伤发生中的作用及地塞米松对NF κB活化的影响 ,制作大鼠烟雾吸入性损伤模型 ,将大鼠随机分为正常对照组、烟雾致伤组及地塞米松治疗组 ,应用免疫组化方法观察伤前及伤后 2、6、12、2 4、48、72h肺组织NF κBP65、IκB α、TNF α、ICAM 1蛋白表达的动态变化。结果显示 ,烟雾吸入性损伤后肺组织NF κBP65、TNF α、ICAM 1蛋白表达升高 ,IκB α表达降低。而地塞米松治疗组则下调NF κBP65、TNF α、ICAM 1表达 ,上调IκB α表达。提示NF κB活化参与了烟雾吸入损害的发生、发展 ,而地塞米松则抑制NF κB活化 ,部分阻断细胞因子及粘附分子产生 ,从而减轻炎症性损害。NF κB活化可能是烟雾吸入性损伤炎症发展的关键点 ,从而为从转录水平作为靶点治疗烟雾吸入性损伤提供了理论依据。

The aim of the study was to explore the role of NF κB activation in the pathogenesis of smoke inhalation injury and to evaluate the effects of dexamethasone on NF κB activation. 130 Wistar rats were inflicted with smoke inhalation injury and randomized equally into the control group, smoke inhalation injury group and dexamethasone treatment group.The expressions of NF κB P 65 ,IκB α,TNF α,and ICAM 1 proteins in the lung tissue were determined by immunohistochemistry at 2,6,12,24,48,72 hours after smoke inhalation injury. The results showed that,after smoke inhalation ,the expressions of NF κBP 65 ,TNF α,and ICAM 1 increased,whereas the expression of IκB α decreased. In the dexamethasone treatment group,the expressions of NF κBP 65 ,TNF α,and ICAM 1 were down regulated, and IκB α was up regulated.These results suggest that NF κB activation may participate in the pathogenesis of smoke inhalation injury.Dexamethasone could suppress NF κB activation, thus partially blocked the production of cytokines and adhesion molecules,and in turn reduced the damage of inflammatory response. Therefore NF κB activation might be a key point in the development of smoke inhalation injury and modulation of activation of NFκB might be a potential therapeutic strategy to treat this injury at the transcription level.