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PLoS One. 2015 Sep 2;10(9):e0137273. doi: 10.1371/journal.pone.0137273. eCollection 2015.

Effects of High-Intensity Swimming on Lung Inflammation and Oxidative Stress in a Murine Model of DEP-Induced Injury.

Author information

1
Department of Physical Therapy, State University of Santa Catarina, Florianopolis, Brazil.
2
Department of Physical Therapy, State University of Santa Catarina, Florianopolis, Brazil; Departments of Medicine (LIM-5 and LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
3
Department of Biological Science, Federal University of Santa Catarina, Florianopolis, Brazil.
4
Department of Physical Therapy, Pampa Federal University, Uruguaiana, Rio Grande do Sul, Brazil.
5
Departments of Medicine (LIM-5 and LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
6
Laboratory of Experimental Neuroscience, Postgraduate Program in Health Science, University of Southern Santa Catarina at Palhoça, Santa Catarina, Brazil.
7
Health Sciences Center, Brazil Lutheran University, Santa Maria, Rio Grande do Sul, Brazil.
8
Department of Biochemistry, Federal University of Santa Catarina, Florianopolis, Brazil.
9
Postgraduate Program in Rehabilitation Sciences, Nove de Julho University, Sao Paulo (UNINOVE), Brazil.

Abstract

Studies have reported that exposure to diesel exhaust particles (DEPs) induces lung inflammation and increases oxidative stress, and both effects are susceptible to changes via regular aerobic exercise in rehabilitation programs. However, the effects of exercise on lungs exposed to DEP after the cessation of exercise are not clear. Therefore, the aim of this study was to evaluate the effects of high-intensity swimming on lung inflammation and oxidative stress in mice exposed to DEP concomitantly and after exercise cessation. Male Swiss mice were divided into 4 groups: Control (n = 12), Swimming (30 min/day) (n = 8), DEP (3 mg/mL-10 μL/mouse) (n = 9) and DEP+Swimming (n = 8). The high-intensity swimming was characterized by an increase in blood lactate levels greater than 1 mmoL/L between 10th and 30th minutes of exercise. Twenty-four hours after the final exposure to DEP, the anesthetized mice were euthanized, and we counted the number of total and differential inflammatory cells in the bronchoalveolar fluid (BALF), measured the lung homogenate levels of IL-1β, TNF-α, IL-6, INF-ϫ, IL-10, and IL-1ra using ELISA, and measured the levels of glutathione, non-protein thiols (GSH-t and NPSH) and the antioxidant enzymes catalase and glutathione peroxidase (GPx) in the lung. Swimming sessions decreased the number of total cells (p<0.001), neutrophils and lymphocytes (p<0.001; p<0.05) in the BALF, as well as lung levels of IL-1β (p = 0.002), TNF-α (p = 0.003), IL-6 (p = 0.0001) and IFN-ϫ (p = 0.0001). However, the levels of IL-10 (p = 0.01) and IL-1ra (p = 0.0002) increased in the swimming groups compared with the control groups, as did the CAT lung levels (p = 0.0001). Simultaneously, swimming resulted in an increase in the GSH-t and NPSH lung levels in the DEP group (p = 0.0001 and p<0.002). We concluded that in this experimental model, the high-intensity swimming sessions decreased the lung inflammation and oxidative stress status during DEP-induced lung inflammation in mice.

PMID:
26332044
PMCID:
PMC4557939
DOI:
10.1371/journal.pone.0137273
[Indexed for MEDLINE]
Free PMC Article

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