小鼠急性肺损伤后肺内CFTR和ENaC的表达变化  

Changes of expression of CFTR and ENaC in lung of mice after acute lung injury

作　　者：蒋进军[1] 高磊[1] 

机构地区：[1]复旦大学附属中山医院呼吸科,上海200032

出　　处：《中国临床医学》2016年第5期554-558,共5页Chinese Journal of Clinical Medicine

基　　金：上海市科学技术委员会重点项目(15DZ1930602);上海市卫生局应用研究项目(20134056)~~

摘　　要：目的:探讨囊性纤维化跨膜调节因子(cystic fibrosis transmembrane conductance regulator,CFTR)氯离子通道和上皮细胞钠通道(epithelial sodium channel,ENaC)蛋白在内毒素诱发急性肺损伤小鼠肺内的表达变化。方法:将内毒素经小鼠气管注入肺内后诱发急性肺损伤,24h、48h、72h后取肺组织,检测其CFTR和ENaC的mRNA浓度变化、肺泡液体清除率、湿干重比。结果:小鼠急性肺损伤后24h、48h、72h,CFTR在肺内的表达均降低(P<0.05)。小鼠急性肺损伤后24h、48h、72h,α-ENaC在肺内表达均降低(P<0.05);β-ENaC、γ-ENaC在急性肺损伤后24h、48h表达降低(P<0.05),而在急性肺损伤后72h恢复正常。小鼠急性肺损伤后24h、48h、72h,肺泡液体清除率和肺湿干重比出现类似的改变。结论:内毒素诱发的小鼠急性肺损伤组织中,CFTR和ENaC的表达均下降,肺泡液体清除率与其一致,肺湿干重的变化与其相反。Objective：To investigate the changes in the expression of cystic fibrosis transmembrane conductance regulator（CFTR）chloride channel and epithelial sodium channel（ENaC）protein in lung of mice with acute lung injury induced by endotoxin.Methods：Lipopolysaccharide（LPS）was instilled into the tracheas of the mice to induce acute lung injury.After24 h,48hand 72 h,the lung tissue was taken to detect the changes in the mRNA levels of ENaC and CFTR,alveolar fluid clearance（AFC）and wet/dry ratio.Results：24h,48 h,and 72 hafter acute lung injury in mice,the expression of CFTR all decreased in the lung（P〈0.05）.24 h,48h,and 72 hafter acute lung injury in mice,the expression ofα-ENaC all decreased in the lung（P〈0.05）.24 hand 48hafter acute lung injury in mice,the expression ofβ-ENaC andγ-ENaC both decreased in the lung（P〈0.05）,but at 72 h,the level returned to normal.24 h,48h,and 72 hafter acute lung injury in mice,the same change occurred in alveolar fluid clearance,but the lung wet/dry ratio increased.Conclusions：In endotoxin-induced acute lung injury in mice,the expression of CFTR and ENaC both decreased,alveolar fluid clearance also decreased but the wet/dry ratio increased.

关 键 词：急性肺损伤 囊性纤维化跨膜调节因子 上皮细胞钠通道 内毒素 肺泡液体清除率 

分 类 号：R563[医药卫生—呼吸系统]