Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses

Abstract Here we investigated whether hydrogen can protect the lung from chronic injury induced by hypoxia/re-oxygenation (H/R). We developed a mouse model in which H/R exposure triggered clinically typical lung injury, involving increased alveolar wall thickening, infiltration by neutrophils, conso...

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Autores principales: Meihong Chen, Jie Zhang, Yun Chen, Yan Qiu, Zi Luo, Sixia Zhao, Lei Du, Dongbo Tian
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Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/7e25d2f0cdc44bd4ac26c158481e8467
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spelling oai:doaj.org-article:7e25d2f0cdc44bd4ac26c158481e84672021-12-02T15:08:48ZHydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses10.1038/s41598-018-26335-22045-2322https://doaj.org/article/7e25d2f0cdc44bd4ac26c158481e84672018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-26335-2https://doaj.org/toc/2045-2322Abstract Here we investigated whether hydrogen can protect the lung from chronic injury induced by hypoxia/re-oxygenation (H/R). We developed a mouse model in which H/R exposure triggered clinically typical lung injury, involving increased alveolar wall thickening, infiltration by neutrophils, consolidation, alveolar hemorrhage, increased levels of inflammatory factors and recruitment of M1 macrophages. All these processes were attenuated in the presence of H2. We found that H/R-induced injury in our mouse model was associated with production of hydroxyl radicals as well as increased levels of colony-stimulating factors and circulating leukocytes. H2 attenuated H/R-induced production of hydroxyl radicals, up-regulation of colony-stimulating factors, and recruitment of neutrophils and M1 macrophages to lung tissues. However, H2 did not substantially affect the H/R-induced increase in erythropoietin or pulmonary artery remodeling. Our results suggest that H2 ameliorates H/R-induced lung injury by inhibiting hydroxyl radical production and inflammation in lungs. It may also prevent colony-stimulating factors from mobilizing progenitors in response to H/R-induced injury.Meihong ChenJie ZhangYun ChenYan QiuZi LuoSixia ZhaoLei DuDongbo TianNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-12 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Meihong Chen
Jie Zhang
Yun Chen
Yan Qiu
Zi Luo
Sixia Zhao
Lei Du
Dongbo Tian
Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses
description Abstract Here we investigated whether hydrogen can protect the lung from chronic injury induced by hypoxia/re-oxygenation (H/R). We developed a mouse model in which H/R exposure triggered clinically typical lung injury, involving increased alveolar wall thickening, infiltration by neutrophils, consolidation, alveolar hemorrhage, increased levels of inflammatory factors and recruitment of M1 macrophages. All these processes were attenuated in the presence of H2. We found that H/R-induced injury in our mouse model was associated with production of hydroxyl radicals as well as increased levels of colony-stimulating factors and circulating leukocytes. H2 attenuated H/R-induced production of hydroxyl radicals, up-regulation of colony-stimulating factors, and recruitment of neutrophils and M1 macrophages to lung tissues. However, H2 did not substantially affect the H/R-induced increase in erythropoietin or pulmonary artery remodeling. Our results suggest that H2 ameliorates H/R-induced lung injury by inhibiting hydroxyl radical production and inflammation in lungs. It may also prevent colony-stimulating factors from mobilizing progenitors in response to H/R-induced injury.
format article
author Meihong Chen
Jie Zhang
Yun Chen
Yan Qiu
Zi Luo
Sixia Zhao
Lei Du
Dongbo Tian
author_facet Meihong Chen
Jie Zhang
Yun Chen
Yan Qiu
Zi Luo
Sixia Zhao
Lei Du
Dongbo Tian
author_sort Meihong Chen
title Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses
title_short Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses
title_full Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses
title_fullStr Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses
title_full_unstemmed Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses
title_sort hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/7e25d2f0cdc44bd4ac26c158481e8467
work_keys_str_mv AT meihongchen hydrogenprotectslungfromhypoxiareoxygenationinjurybyreducinghydroxylradicalproductionandinhibitinginflammatoryresponses
AT jiezhang hydrogenprotectslungfromhypoxiareoxygenationinjurybyreducinghydroxylradicalproductionandinhibitinginflammatoryresponses
AT yunchen hydrogenprotectslungfromhypoxiareoxygenationinjurybyreducinghydroxylradicalproductionandinhibitinginflammatoryresponses
AT yanqiu hydrogenprotectslungfromhypoxiareoxygenationinjurybyreducinghydroxylradicalproductionandinhibitinginflammatoryresponses
AT ziluo hydrogenprotectslungfromhypoxiareoxygenationinjurybyreducinghydroxylradicalproductionandinhibitinginflammatoryresponses
AT sixiazhao hydrogenprotectslungfromhypoxiareoxygenationinjurybyreducinghydroxylradicalproductionandinhibitinginflammatoryresponses
AT leidu hydrogenprotectslungfromhypoxiareoxygenationinjurybyreducinghydroxylradicalproductionandinhibitinginflammatoryresponses
AT dongbotian hydrogenprotectslungfromhypoxiareoxygenationinjurybyreducinghydroxylradicalproductionandinhibitinginflammatoryresponses
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