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作 者:卢红艳[1] 常立文[1] 李文斌[1] 姜娜[1] 彭琼玲[1] 蔡成[1] 刘敬[1]
机构地区:[1]华中科技大学同济医学院同济医院儿科,湖北武汉430030
出 处:《基础医学与临床》2007年第5期553-556,共4页Basic and Clinical Medicine
摘 要:目的探讨水通道蛋白5(AQP5)在早产大鼠及吸高氧过程中的肺动态表达。方法剖宫术取出孕21d SD早产鼠,于12~24h内随机分为对照组和高氧组。分别在1、4、7、10和14d时提取肺组织,RT-PCR测定AQP5 mRNA表达,免疫组化和Western blot检测AQP5蛋白的表达。结果早产大鼠生后肺组织AQP5表达不断增强,其阳性染色主要定位于Ⅰ型肺泡上皮细胞。高氧暴露1d时,仅肺组织AQP5 mRNA表达显著高于对照组(P<0·05),而高氧暴露4、7、10及14d时,其mRNA及蛋白表达均明显减少(P<0·05或P<0·01)。结论AQP5通过调节肺水平衡,在早产大鼠肺泡化形成的关键时期发挥重要作用;高氧暴露导致AQP5表达下调是促使肺损伤发生、发展的重要因素。Objective To explore the expression of lung Aquaporin.5 (AQPS) in premature rats and during the process of inhaling hyperoxia. Methods Gestation 21 day Sprague-Dawley (SD) fetuses ( term = 22 day) were randomly divideal into control group and hyperoxia group 12 - 24 h after birth. Hypreoxia group was exposed to about 85% oxygen. After 1 to 14 days of exposure, lung tissue was isolated and AQP5 mRNA was detected by RT-PCR. Immunohistochemistry and Western-blot was used to detect AQP5 protein. Results The expression of lung AQP5 in premature rats persistently increased after birth, and the positive staining was restricted to the type I alveolar epithelial cells. Compared with control group, the AQP5 mRNA in hyperoxia group of day 1 increased significantly ( P 〈 0. 05 ), but after exposure to hyperoxia for 4 to 14 days, the AQP5 expression resulted in a decrease of mRNA and protein(P 〈 0. 05 or P 〈 0. 01 ). Conclusion AQP5 may play a key role in the alveolar period of premature rats. Hyperoxia down-regulates the AQP5 expression, this might be an important factor for the development of hyperoxia lung injury.
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