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

被引:20
作者
Avila, Leonardo C. M. [1 ]
Bruggemann, Thayse R. [1 ,2 ]
Bobinski, Franciane [3 ]
da Silva, Morgana Duarte [4 ]
Oliveira, Regiane Carvalho [2 ]
Martins, Daniel Fernandes [5 ]
Mazzardo-Martins, Leidiane [3 ]
Medeiros Frescura Duarte, Marta Maria [6 ]
de Souza, Luiz Felipe [7 ]
Dafre, Alcir [7 ]
Vieira, Rodolfo de Paula [8 ]
Soares Santos, Adair Roberto [3 ]
Bonorino, Kelly Cattelan [1 ]
Kunzler, Deborah de C. Hizume [1 ,2 ]
机构
[1] Univ Estado Santa Catarina, Dept Phys Therapy, Florianopolis, SC, Brazil
[2] Univ Sao Paulo, Sch Med, Dept Med LIM 5 & LIM 20, BR-05508 Sao Paulo, Brazil
[3] Univ Estado Santa Catarina, Dept Biol Sci, Florianopolis, SC, Brazil
[4] Pampa Fed Univ, Dept Phys Therapy, Uruguaiana, RS, Brazil
[5] Univ Southern Santa Catarina, Postgrad Program Hlth Sci, Lab Expt Neurosci, Palhoca, SC, Brazil
[6] Brazil Lutheran Univ, Hlth Sci Ctr, Santa Maria, RS, Brazil
[7] Univ Fed Santa Catarina, Dept Biochem, Florianopolis, SC, Brazil
[8] Nove de Julho Univ, Sao Paulo UNINOVE, Postgrad Program Rehabil Sci, Bauru, SP, Brazil
关键词
DIESEL EXHAUST PARTICLES; AEROBIC EXERCISE; AIR-POLLUTION; CYTOCHROME-P450; 1A1; PARTICULATE MATTER; PERIPHERAL-BLOOD; EPITHELIAL-CELLS; GENE-EXPRESSION; TERM EXPOSURE; MOUSE MODEL;
D O I
10.1371/journal.pone.0137273
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
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 mu L/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-1 beta, TNF-alpha, IL-6, INF-(sic), 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-1 beta (p = 0.002), TNF-alpha (p = 0.003), IL-6 (p = 0.0001) and IFN-(sic) (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.
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页数:15
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