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目的探讨高氧损伤状态下,肺组织内水通道蛋白1(AQP1)和AQP5 mRNA的动态变化规律及其在肺水肿中的作用。方法新生鼠320只,依据吸氧浓度(FiO2)分组:实验组1(FiO20.8)、实验组2(FiO20.6)、实验组3(FiO20.4)、空气对照组(FiO20.21)。每组分别于实验后1、3、5、7、14d行AQP1 mRNA、AQP5 mRNA RT-PCR检测,同时检测肺组织Evans蓝含量。结果高氧各组肺组织Evans蓝含量与空气组相比均显著增加,并随吸氧浓度、暴露时间的延长而增加。新生大鼠肺组织AQP1(高氧3d时)、AQP5(高氧5d时)基因表达明显低于对照组(F1=53.004,P=0.008;F2=16.617,P=0.01),总趋势上AQP1、AQP5 mRNA的表达实验组1、实验组2、实验组3依次降低。结论AQP1、AQP5 mRNA在高氧肺损伤时表达降低,并与肺水肿的严重程度密切相关。
Objective To investigate the dynamic changes of AQP1 and AQP5 mRNA and their roles in pulmonary edema under hyperoxia injury. Methods 320 newborn rats were divided into three groups according to FiO2: FiO20.8, FiO20.6, FiO20.4, FiO20.21, . AQP1 mRNA and AQP5 mRNA were detected by RT-PCR at 1, 3, 5, 7 and 14 days after the experiment in each group. Evans blue content in lung tissue was also detected. Results Compared with the air group, the content of Evans blue in lungs of all groups increased significantly, and increased with the increase of oxygen concentration and exposure time. The expression of AQP1, AQP1 and AQP5 in lung tissue of neonatal rats was significantly lower than that of the control group (F1 = 53.004, P = 0.008; F2 = 16.617, P = 0.01) AQP5 mRNA expression in experimental group 1, experimental group 2, experimental group 3 in turn decreased. Conclusion The expression of AQP1 and AQP5 mRNA is decreased in hyperoxia-induced lung injury and is closely related to the severity of pulmonary edema.