水通道蛋白-1和水通道蛋白-5在高原肺水肿大鼠模型中的表达及高压氧暴露的影响
Expression of Aquaporin-1 and Aquaporin-5 in a Rat Model of High-Altitude Pulmonary Edema and the Effect of Hyperbaric Oxygen Exposure.
作者信息
Tan Jiewen, Gao Chunjin, Wang Cong, Ma Linlin, Hou Xiaomin, Liu Xuehua, Li Zhuo
机构信息
Department of Rehabilitation Medicine, XinHua College, Sun Yat-Sen University, Guangzhou, China.
Department of Hyperbaric Oxygen, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
出版信息
Dose Response. 2020 Oct 30;18(4):1559325820970821. doi: 10.1177/1559325820970821. eCollection 2020 Oct-Dec.
OBJECTIVE
To investigate the therapeutic roles of hyperbaric oxygen exposure on high-altitude pulmonary edema and to determine whether aquaporin-1 and aquaporin-5 were involved in the pathogenesis of HAPE in rats.
METHODS
Rats were divided into 5 groups: The control group, the HAPE group (HAPE model), the HBO group (hyperbaric oxygen exposure), the NBO group (normobaric oxygen exposure), and the NA group (normal air exposure). Western blot and real-time PCR were used to analyze the pulmonary expressions of AQP1 and AQP5. The wet-to-dry (W/D) weight ratio and the morphology of the lung were also examined.
RESULTS
The lung W/D weight ratio in the HAPE group was increased compared with the control group. The injury score in the HBO group was noticeably lower than that in the control group. The mRNA and proteins expressions of AQP1 and AQP5 were significantly downregulated in the HAPE group.
CONCLUSIONS
Oxygen exposure alleviated high-altitude hypobaric hypoxia-induced lung injury in rats. Additionally, HBO therapy had significant advantage on interstitial HAPE.
目的
探讨高压氧暴露对高原肺水肿的治疗作用，并确定水通道蛋白-1和水通道蛋白-5是否参与大鼠高原肺水肿的发病机制。
方法
将大鼠分为5组：对照组、高原肺水肿组（高原肺水肿模型）、高压氧组（高压氧暴露）、常压氧组（常压氧暴露）和常氧组（常氧暴露）。采用蛋白质免疫印迹法和实时荧光定量聚合酶链反应分析肺组织中水通道蛋白-1和水通道蛋白-5的表达。同时检测肺组织湿干重比及肺组织形态学变化。
结果
高原肺水肿组肺组织湿干重比高于对照组。高压氧组损伤评分明显低于对照组。高原肺水肿组水通道蛋白-1和水通道蛋白-5的mRNA和蛋白表达均明显下调。
结论
氧暴露可减轻大鼠高原低压低氧性肺损伤。此外，高压氧治疗对间质性高原肺水肿具有显著优势。
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