高原肺水肿
水通道蛋白1
肺水肿
医学
缺氧(环境)
高压氧
肺
水肿
发病机制
麻醉
高海拔对人类的影响
免疫印迹
活性氧
内科学
内分泌学
病理
氧气
化学
水道
解剖
生物化学
入口
机械工程
有机化学
工程类
基因
作者
Jiewen Tan,Chunjin Gao,Cong Wang,Linlin Ma,Xiaomin Hou,Xuehua Liu,Zhuo Li
出处
期刊:Dose-response
[SAGE Publishing]
日期:2020-10-01
卷期号:18 (4)
被引量:18
标识
DOI:10.1177/1559325820970821
摘要
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.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.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.Oxygen exposure alleviated high-altitude hypobaric hypoxia-induced lung injury in rats. Additionally, HBO therapy had significant advantage on interstitial HAPE.
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