THE ROLE OF NF-?B ACTIVATION IN THE PATHOGENESIS OF SMOKE INHALATION INJURY AND THE EFFECTS OF DEXAMETHASONE ON IT
- VernacularTitle:NF-?B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
- Author:
Wenjun LI
;
Zongcheng YANG
;
Tianpen JI
- Publication Type:Journal Article
- Keywords:
smoke inhalation injury;
NF kappa B;
dexamethasone;
I kappa B;
tumor necrosis factor;
intercellular adhesion molecule 1
- From:
Medical Journal of Chinese People's Liberation Army
1982;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the study was to explore the role of NF ?B activation in the pathogenesis of smoke inhalation injury and to evaluate the effects of dexamethasone on NF ?B 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 ?B P 65 ,I?B ?,TNF ?,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 ?BP 65 ,TNF ?,and ICAM 1 increased,whereas the expression of I?B ? decreased. In the dexamethasone treatment group,the expressions of NF ?BP 65 ,TNF ?,and ICAM 1 were down regulated, and I?B ? was up regulated.These results suggest that NF ?B activation may participate in the pathogenesis of smoke inhalation injury.Dexamethasone could suppress NF ?B activation, thus partially blocked the production of cytokines and adhesion molecules,and in turn reduced the damage of inflammatory response. Therefore NF ?B activation might be a key point in the development of smoke inhalation injury and modulation of activation of NF?B might be a potential therapeutic strategy to treat this injury at the transcription level.
