Abstract
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-1β, TGF-β, TNF-α, CXCL-1, IL-17, MMP-9, MPO, NE, and sirt-1; and the BALF levels of CXCL-1, IL-17, TGF-β, IL-10, IL-1β, and TNF-α 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-1β, TNF-α IL-17, and TGF-β but upregulated BALF levels of IL-10. AE decreased IL-1β, TGF-β, TNF-α, 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-β, NE, and MMP-9 expression and activating IL-10 and sirt-1 expression.
Highlights
The prevalence of obesity is increasing drastically and its prevalence markedly upregulates the incidence of many complications such as chronic obstructive pulmonary disease (COPD), asthma, and pulmonary fibrosis (Bianco et al, 2017; Liu et al, 2017; Murtha et al, 2017; Rathinasabapathy et al, 2018; Bluher, 2019)
Forty-eight male C57BL/6 mice were randomly divided into four groups: (1) chow (Ch) group, where the mice were fed a chow diet for 16 weeks; (2) chow diet plus exercise (CE) group, where the mice were fed a chow diet for 16 weeks and forced to train in the last 8 weeks; (3) the obesity (Ob) group, where the mice were fed a high-fat diet (HFD) for 16 weeks; and (4) the obesity plus exercise (OE) group, where the mice were fed a HFD for 16 weeks and forced to train in the last 8 weeks
HFD markedly increased the number of neutrophils in the lung, while aerobic exercise (AE) markedly decreased the number of neutrophils in obese mice (Figure 1)
Summary
The prevalence of obesity is increasing drastically and its prevalence markedly upregulates the incidence of many complications such as chronic obstructive pulmonary disease (COPD), asthma, and pulmonary fibrosis (Bianco et al, 2017; Liu et al, 2017; Murtha et al, 2017; Rathinasabapathy et al, 2018; Bluher, 2019). Obesity results in insulin resistance, vitamin D deficiency, and increased expression of fibrogenic factors including TGF-β, and proinflammatory cytokines such as TNF-α and C-reactive protein; these changes cause pulmonary fibrosis (Wortsman et al, 2000; Ford et al, 2005; Botella-Carretero et al, 2007; Vimaleswaran et al, 2013; Han et al, 2021). Insulin resistance mediates pulmonary fibrosis via the TGF-β pathway (Park et al, 2019). Inflammatory cytokines, including TNF-α and IL-1β, and immune cells, including neutrophils, are important causes of pulmonary fibrosis (Stockley, 2002; Thannickal et al, 2004). Previous 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
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