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Amelioration of Ambient Particulate Matter (PM(2.5))-Induced Lung Injury in Rats by Aerobic Exercise Training

Ambient particulate matter (PM(2.5)), as an inflammation-inducing factor, increases the prevalence of lung injury. The aim of this study was to examine the protective effect and mechanism of aerobic exercise on PM(2.5) exposure-induced lung injury. Forty Wistar rats were randomly divided into four g...

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Autores principales: Qin, Fei, Fan, Zhengzheng, Xu, Minxiao, Wang, Zhongwei, Dong, Yanan, Qu, Chaoyi, Cui, Shuqiang, Zhao, Lina, Zhao, Jiexiu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8576392/
https://www.ncbi.nlm.nih.gov/pubmed/34764879
http://dx.doi.org/10.3389/fphys.2021.731594
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author Qin, Fei
Fan, Zhengzheng
Xu, Minxiao
Wang, Zhongwei
Dong, Yanan
Qu, Chaoyi
Cui, Shuqiang
Zhao, Lina
Zhao, Jiexiu
author_facet Qin, Fei
Fan, Zhengzheng
Xu, Minxiao
Wang, Zhongwei
Dong, Yanan
Qu, Chaoyi
Cui, Shuqiang
Zhao, Lina
Zhao, Jiexiu
author_sort Qin, Fei
collection PubMed
description Ambient particulate matter (PM(2.5)), as an inflammation-inducing factor, increases the prevalence of lung injury. The aim of this study was to examine the protective effect and mechanism of aerobic exercise on PM(2.5) exposure-induced lung injury. Forty Wistar rats were randomly divided into four groups: sedentary+PM(2.5) exposure, exercise+PM(2.5) exposure, sedentary, and exercise groups. All rats in the exercise-related groups underwent 8-week aerobic interval treadmill training (5daysweek(−1), 1hday(−1)). PM-exposed rats were exposed to ambient PM(2.5) (6h day(−1)) for 3weeks after the 8-week exercise intervention. Then, ventilation function, histopathological changes, and inflammation responses of pulmonary tissue were examined. Results showed that PM(2.5) exposure induced lung injury as manifested by decreased pulmonary function, abnormal histopathological changes, and increased pro-inflammatory cytokine levels (tumor necrosis factor-α and Interleukin-1α). Aerobic exercise alleviated the airway obstruction, reduced respiratory muscle strength, bronchial mucosal exfoliation, ultrastructure damage, and inflammatory responses induced by PM(2.5) in exercise-related groups. The benefits of exercise were related with the downregulation of p38-mitogen-activated protein kinase (MAPK), and the subsequent inhibition of the pathways of the cyclooxygenase 2 (COX-2) product, prostaglandin E(2) (PGE(2)). Thus, pre-exercise training may be an effective way to protect against PM(2.5)-induced lung inflammatory injury in rats.
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spelling pubmed-85763922021-11-10 Amelioration of Ambient Particulate Matter (PM(2.5))-Induced Lung Injury in Rats by Aerobic Exercise Training Qin, Fei Fan, Zhengzheng Xu, Minxiao Wang, Zhongwei Dong, Yanan Qu, Chaoyi Cui, Shuqiang Zhao, Lina Zhao, Jiexiu Front Physiol Physiology Ambient particulate matter (PM(2.5)), as an inflammation-inducing factor, increases the prevalence of lung injury. The aim of this study was to examine the protective effect and mechanism of aerobic exercise on PM(2.5) exposure-induced lung injury. Forty Wistar rats were randomly divided into four groups: sedentary+PM(2.5) exposure, exercise+PM(2.5) exposure, sedentary, and exercise groups. All rats in the exercise-related groups underwent 8-week aerobic interval treadmill training (5daysweek(−1), 1hday(−1)). PM-exposed rats were exposed to ambient PM(2.5) (6h day(−1)) for 3weeks after the 8-week exercise intervention. Then, ventilation function, histopathological changes, and inflammation responses of pulmonary tissue were examined. Results showed that PM(2.5) exposure induced lung injury as manifested by decreased pulmonary function, abnormal histopathological changes, and increased pro-inflammatory cytokine levels (tumor necrosis factor-α and Interleukin-1α). Aerobic exercise alleviated the airway obstruction, reduced respiratory muscle strength, bronchial mucosal exfoliation, ultrastructure damage, and inflammatory responses induced by PM(2.5) in exercise-related groups. The benefits of exercise were related with the downregulation of p38-mitogen-activated protein kinase (MAPK), and the subsequent inhibition of the pathways of the cyclooxygenase 2 (COX-2) product, prostaglandin E(2) (PGE(2)). Thus, pre-exercise training may be an effective way to protect against PM(2.5)-induced lung inflammatory injury in rats. Frontiers Media S.A. 2021-10-26 /pmc/articles/PMC8576392/ /pubmed/34764879 http://dx.doi.org/10.3389/fphys.2021.731594 Text en Copyright © 2021 Qin, Fan, Xu, Wang, Dong, Qu, Cui, Zhao and Zhao. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Qin, Fei
Fan, Zhengzheng
Xu, Minxiao
Wang, Zhongwei
Dong, Yanan
Qu, Chaoyi
Cui, Shuqiang
Zhao, Lina
Zhao, Jiexiu
Amelioration of Ambient Particulate Matter (PM(2.5))-Induced Lung Injury in Rats by Aerobic Exercise Training
title Amelioration of Ambient Particulate Matter (PM(2.5))-Induced Lung Injury in Rats by Aerobic Exercise Training
title_full Amelioration of Ambient Particulate Matter (PM(2.5))-Induced Lung Injury in Rats by Aerobic Exercise Training
title_fullStr Amelioration of Ambient Particulate Matter (PM(2.5))-Induced Lung Injury in Rats by Aerobic Exercise Training
title_full_unstemmed Amelioration of Ambient Particulate Matter (PM(2.5))-Induced Lung Injury in Rats by Aerobic Exercise Training
title_short Amelioration of Ambient Particulate Matter (PM(2.5))-Induced Lung Injury in Rats by Aerobic Exercise Training
title_sort amelioration of ambient particulate matter (pm(2.5))-induced lung injury in rats by aerobic exercise training
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8576392/
https://www.ncbi.nlm.nih.gov/pubmed/34764879
http://dx.doi.org/10.3389/fphys.2021.731594
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