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肺巨噬细胞参与复发性潜水导致的肺损伤。

Lung macrophages are involved in lung injury secondary to repetitive diving.

机构信息

Department of Navy Aviation Medicine, Faculty of Naval Medicine, the Naval Military Medical University, Shanghai 200433, China.

Department of Respiratory Diseases, Hongkou Branch of Changhai Hospital, the Naval Military Medical University, Shanghai 200081, China.

出版信息

J Zhejiang Univ Sci B. 2020;21(8):646-656. doi: 10.1631/jzus.B1900687.

Abstract

This study aimed to establish an animal model of decompression-induced lung injury (DILI) secondary to repetitive diving in mice and explore the role of macrophages in DILI and the protective effects of high-concentration hydrogen (HCH) on DILI. Mice were divided into three groups: control group, DILI group, and HCH group. Mice were exposed to hyperbaric air at 600 kPa for 60 min once daily for consecutive 3 d and then experienced decompression. In HCH group, mice were administered with HCH (66.7% hydrogen and 33.3% oxygen) for 60 min after each hyperbaric exposure. Pulmonary function tests were done 6 h after decompression; the blood was harvested for cell counting; the lung tissues were harvested for the detection of inflammatory cytokines, hematoxylin and eosin (HE) staining, and immunohistochemistry; western blotting and polymerase chain reaction (PCR) were done for the detection of markers for M1 and M2 macrophages. Our results showed that bubbles formed after decompression and repeated hyperbaric exposures significantly reduced the total lung volume and functional residual volume. Moreover, repetitive diving dramatically increased proinflammatory factors and increased the markers of both M1 and M2 macrophages. HCH inhalation improved lung function to a certain extent, and significantly reduced the pro-inflammatory factors. These effects were related to the reduction of M1 macrophages as well as the increase in M2 macrophages. This study indicates that repetitive diving damages lung function and activates lung macrophages, resulting in lung inflammation. HCH inhalation after each diving may be a promising strategy for the prevention of DILI.

摘要

本研究旨在建立一种重复性潜水致减压性肺损伤(DILI)的小鼠动物模型,探讨巨噬细胞在 DILI 中的作用以及高浓度氢气(HCH)对 DILI 的保护作用。将小鼠分为三组:对照组、DILI 组和 HCH 组。小鼠每日暴露于 600 kPa 的高压空气中 60 分钟,连续 3 天,然后进行减压。在 HCH 组中,每次高压暴露后,小鼠接受 HCH(66.7%氢气和 33.3%氧气)治疗 60 分钟。减压后 6 小时进行肺功能测试;采集血液进行细胞计数;采集肺组织检测炎症细胞因子、苏木精和伊红(HE)染色和免疫组织化学;Western blot 和聚合酶链反应(PCR)用于检测 M1 和 M2 巨噬细胞的标志物。我们的结果表明,减压和重复高压暴露后形成的气泡显著降低了总肺容积和功能残气量。此外,重复性潜水显著增加了促炎因子,并增加了 M1 和 M2 巨噬细胞的标志物。HCH 吸入在一定程度上改善了肺功能,并显著降低了促炎因子。这些作用与 M1 巨噬细胞的减少以及 M2 巨噬细胞的增加有关。本研究表明,重复性潜水会损害肺功能并激活肺巨噬细胞,导致肺炎症。每次潜水后吸入 HCH 可能是预防 DILI 的一种有前途的策略。

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