Aerobic Exercise Alleviates Inflammation, Oxidative Stress, and Apoptosis in Mice with Chronic Obstructive Pulmonary Disease

文献类型： 外文期刊

第一作者： Wang, Xishuai

作者： Wang, Xishuai;Wang, Zhiqing;Tang, Donghui;Wang, Xishuai

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关键词： exercise; COPD; pulmonary fibrosis; emphysema; pulmonary inflammation; oxidative stress injury

期刊名称：INTERNATIONAL JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE （ 影响因子：3.355； 五年影响因子：3.739 ）

ISSN： 1178-2005

年卷期： 2021 年 16 卷

页码：

收录情况： SCI

摘要： Background: Chronic inflammation, oxidative stress, and apoptosis play critical roles in chronic obstructive pulmonary disease (COPD) pathogenesis. Here, we attempted to determine whether aerobic exercise (AE) could improve COPD by counteracting the COPD-associated inflammatory response, oxidative stress, and apoptosis in mice. Methods: Thirty male ICR mice were assigned into one of three groups: control (Con), COPD, and COPD + AE. COPD was simulated by intratracheal injection of lipopolysaccharide (LPS) for 4 weeks. Low-intensity AE was performed for 4 weeks. Bronchoalveolar lavage fluid (BALF) cell counts and the levels of inflammatory cytokine in BALF and serum were detected. Hematoxylin and eosin (HE), Masson trichrome, and Sirius Red staining as well as terminal deoxynucleotidyl transferase dUTP nick end labeling were performed to identify the degree of pulmonary emphysema, bronchial mucus cell hyperplasia, pulmonary fibrosis, and cell apoptosis. Oxidative stress parameters were measured. Furthermore, gene expression levels for the CXCL1, IL-1 beta, IL-10, IL-17, matrix metalloproteinase (MMP)9, TGF-beta, TNF-alpha, and silent information regulator (sirt)1 were detected in mice lung tissues. Results: AE improved LPS-induced emphysema, pulmonary fibrosis, bronchial mucus cell hyperplasia, bronchoconstriction, and cell apoptosis. AE prevented an LPS-induced increase in the total cell, neutrophil, and macrophage counts. AE decreased malondialdehyde (MDA) and myeloperoxidase (MPO) levels but increased glutathione (GSH) and superoxide dismutase (SOD) levels. AE decreased BALF levels of IL-1 beta, TNF-alpha, and TGF-beta but increased BALF IL-10 levels. AE suppressed the gene expression levels of pro-inflammatory factors CXCL1, IL-1 beta, IL-17, and TNF-alpha and profibrotic factors MMP-9 and TGF-beta but activated those of anti-inflammatory factor IL-10 and lung-protective factor sirt1. Conclusion: AE is a potential therapeutic approach for COPD. AE improved emphysema, bronchial mucus cell hyperplasia, and pulmonary fibrosis in mice with COPD by alleviating the inflammatory response, oxidative stress injury, and cell apoptosis as well as activating sirt1.

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