水通道蛋白1在高氧肺损伤中的表达变化

目的：探讨AQP1在高氧肺损伤中的表达变化及其在肺水肿中的作用机制。方法：将2周左右Wistar大鼠32只随机分为空气对照组和高氧暴露不同时间组，分别置于常压高氧仓中（氧体积分数〉1．95）和常压空气中，采用RT—PCR和免疫组化方法观察AQP1的分布和表达变化，并对支气管肺泡灌洗液（BALF）中的蛋白含量、肺通透系数、肺湿／干重比（W／D）及肺组织病理学改变也进行了对比分析。结果：高氧组3天时肺组织出现水肿、出血、炎性细胞浸润，7天时炎性改变进一步加重，14天时开始出现肺纤维化的倾向。W／D值、BALF蛋白含量和肺通透系数在3、7、14天时均高于空气组。肺组织AQP1mRNA的表达在高氧3、7和14天时均明显低于空气组（P〈0．05），随暴露时间延长持续下降，在14天时有所恢复；免疫组化显示AQP1主要分布在支气管和肺泡壁的毛细血管内皮细胞及间质细胞，高氧损伤后肺AQP1的表达部位未发生改变。AQP1的蛋白表达变化与其mRNA表达变化结果是一致的。结论：高氧性肺损伤可能存在AQPs的基因表达调控失衡，这可能是高氧性肺损伤肺水肿形成的原因之一。

The expression change of aquaporin 1 in hyperoxic lung injury

Objective:To study the expression change of aquaporin1 in hyperoxia-induced lung injury and the mechanism of action in lung oedema.Methods:Thirty-two juvenile(about two weeks) Wistar rats were randomly divided into breathing room-air group(n =8) and hyperoxia exposure group(n =8 at 3,7 and 14days respectively).The rats were continuously exposed to oxygen(O2>0.95)or room air(O2=0.21,respectively.The distributions of AQP1 in the lung tissues were detected by immunohistochemistry and their mRNA expressions were measured by RT-PCR.In addition,the wet-to-dry weight ratio(W/D),the protein content of bronchoalveolar lavage fluid(BALF),lung leak index,histological changes of hyperoxia-induced lung injury were measured respectively.Results:Light microscopic findings in the hyperoxia group including oedema,hemorrhage and extensive inflammatory cells in the lungs were observed.The lung W/D?the protein content in BALF and the lung leak index in hyperoxia group were significantly higher than those in room air group.The expressions of AQP1 mRNA in the lungs were significantly decreased at 3d of hyperoxia-exposure,minimized at 7d and increased from 14d(P<0.05).Immunohistochemistry for AQP1 was seen primarily in microvascular endothelia cells around bronchus and alveolus,and interstitial cells;the positive regions were similar for room-air group and hyperoxia group.The dynamic changes of AQP1 protein level coincided with the changes of AQP1 mRNA expression.Conclusion:Hyperoxic lung injury may induce regulative unbalance of aquaporins expression,maybe it is one of the reasons for lung oedema caused by hyperoxic lung injury.