摘要
目的探讨胸部开放伤后胸腔海水浸泡致急性肺损伤（ALI）犬肺组织内细胞凋亡及相关基因表达的变化及意义。方法制备胸部开放伤后胸腔海水浸泡致Au犬模型作为实验组，以单纯胸部开放伤犬作为对照组。采用TUNEL法检测实验组及对照组犬肺组织细胞凋亡的变化，采用免疫组化检测Fas／FasL、核转录因子（NF—κB）蛋白表达的变化。结果胸腔海水浸泡致ALI犬肺内肺泡上皮细胞和肺毛细血管内皮细胞凋亡数明显增加，显著高于对照组（P〈0．05）。实验组犬肺组织内Fas（2717±312）、FasL（1994±104）、NF—κB（3651±125）蛋白表达较对照组[（1070±134）、（823±105）、（1116±108）]显著增加（P〈0．05）。结论肺内细胞凋亡参与胸部开放伤后胸腔海水浸泡致ALI的发病，Fas／FasL是介导肺内细胞凋亡的重要途径之一。
Objective To explore apopiosis of lung tissues in dogs with acute lung injury coupled with thoracic seawater immersion and changes in gene expression following open chest injury. Methods The dogs with acute lung injury induced by open chest injury coupled with thoracic seawater immersion were used as the experimental group, and the dogs with just simple open chest injury were used as control animals. Tunel method was used to detect changes in the apoptosis of lung tissues of both animal groups, and immunochemistry was applied to detect changes in the expressions of Fas/FasL and nuclear factor-k-gene binding （NF-κB）. Results Apoptosis of alveolar epithelial cells and pulmonary vascular endothelial cells in the animals of the experimental group was significantly increased, when compared with that of the control group （ P 〈 0.05 ）. The expressions of Fas/FasL and NF-κB in the experimental dogs were also increased considerably, when compared with those of the control group （ P 〈 0. 05 ）. Conclusions Apoptosis of alveolar epithelial ceils and pulmonary endothelial cells was involved in the development of acute lung injury induced by open chest injury coupled with thoracic seawater immersion, and Fas/FasL system might be one of the important factors contributing to the apoptosis of lung tissues,
出处
《中华航海医学与高气压医学杂志》
CAS
CSCD
北大核心
2012年第1期13-16,共4页
Chinese Journal of Nautical Medicine and Hyperbaric Medicine
