Aerobic Exercise Improves Pulmonary Fibrosis by Improving Insulin Resistance and Inflammation in Obese Mice

文献类型： 外文期刊

第一作者： Wang, Xishuai

作者： Wang, Xishuai;Tang, Donghui;Wang, Xishuai;Yi, Xuejie

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关键词： obesity; pulmonary fibrosis; inflammation; oxidative stress; insulin resistance; exercise

期刊名称：FRONTIERS IN PHYSIOLOGY （ 影响因子：4.755； 五年影响因子：5.316 ）

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年卷期： 2022 年 12 卷

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收录情况： SCI

摘要： BackgroundPrevious studies have demonstrated that obesity is associated with pulmonary fibrosis. We attempted to identify whether regular aerobic exercise (AE) can protect against high-fat diet (HFD)-associated pulmonary fibrosis. MethodsForty-eight C57BL/6 mice were randomly assigned to four groups: chow group (Ch), chow plus exercise group (CE), obesity group (Ob), and obesity plus exercise group (OE). The mice were fed either an HFD or a chow diet for 16 weeks, and low-intensity aerobic exercise (AE) was performed in the last 8 weeks. We measured the degree of pulmonary fibrosis; pulmonary inflammation; oxidative stress parameters; insulin resistance-related indicators; the number of inflammatory cells in bronchoalveolar lavage fluid (BALF); the mRNA expression levels of IL-10, IL-1 beta, TGF-beta, TNF-alpha, CXCL-1, IL-17, MMP-9, MPO, NE, and sirt-1; and the BALF levels of CXCL-1, IL-17, TGF-beta, IL-10, IL-1 beta, and TNF-alpha in lung tissue. ResultsAE in obese mice protected against obesity-associated pulmonary fibrosis, chronic inflammation, pro-oxidative/antioxidative imbalance, and insulin resistance. AE ameliorated the HFD-induced inflammatory response and neutrophil infiltration in the lung. AE downregulated BALF levels of CXCL-1, IL-1 beta, TNF-alpha IL-17, and TGF-beta but upregulated BALF levels of IL-10. AE decreased IL-1 beta, TGF-beta, TNF-alpha, CXCL-1, IL-17, MMP-9, MPO, and NE mRNA expression levels but upregulated IL-10 and sirt-1 mRNA expression levels in the lung. ConclusionsAE protects against HFD-induced pulmonary fibrosis by improving obesity-associated insulin resistance, chronic low-grade inflammation, and pro-oxidative/antioxidative imbalance. AE improved HFD-induced pulmonary fibrosis by suppressing IL-17, TGF-beta, NE, and MMP-9 expression and activating IL-10 and sirt-1 expression.

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