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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 6572714, 13 pages
Research Article

Exercise Inhibits the Effects of Smoke-Induced COPD Involving Modulation of STAT3

1Nove de Julho University, São Paulo, SP, Brazil
2Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), School of Medical Sciences of São José dos Campos Humanitas and Universidade Brasil, São Paulo, SP, Brazil
3Institute of Physical Activity Sciences and Sports, Post-Graduate Program in Human Movement Sciences, Cruzeiro do Sul University, São Paulo, SP, Brazil
4Institute for Memory Impairments and Neurological Disorders (MIND Institute), University of California, Irvine, CA, USA
5Laboratory of Experimental Therapeutics (LIM 20), Department of Medicine, School of Medicine, University of Sao Paulo, São Paulo, SP, Brazil
6Respiratory Pharmacology Group, Airway Disease, National Heart and Lung Institute, Imperial College London, London, UK

Correspondence should be addressed to Rodolfo Paula Vieira; rb.moc.oohay@anelerdor

Received 19 May 2017; Revised 9 August 2017; Accepted 29 August 2017; Published 18 October 2017

Academic Editor: Julien S. Baker

Copyright © 2017 Maysa Alves Rodrigues Brandao-Rangel et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Purpose. Evaluate the participation of STAT3 in the effects of aerobic exercise (AE) in a model of smoke-induced COPD. Methods. C57Bl/6 male mice were divided into control, Exe, COPD, and COPD+Exe groups. Smoke were administered during 90 days. Treadmill aerobic training begun on day 61 until day 90. Pulmonary inflammation, systemic inflammation, the level of lung emphysema, and the airway remodeling were evaluated. Analysis of integral and phosphorylated expression of STAT3 by airway epithelial cells, peribronchial leukocytes, and parenchymal leukocytes was performed. Results. AE inhibited smoke-induced accumulation of total cells (), lymphocytes (), and neutrophils () in BAL, as well as BAL levels of IL-1β (), CXCL1 (), IL-17 (), and TNF-α (), while increased the levels of IL-10 (). AE also inhibited smoke-induced increases in total leukocytes (), neutrophils (), lymphocytes (), and monocytes () in blood, as well as serum levels of IL-1β (), CXCL1 (), IL-17 (), and TNF-α (), while increased the levels of IL-10 (). AE reduced smoke-induced emphysema () and collagen fiber accumulation in the airways (). AE reduced smoke-induced STAT3 and phospho-STAT3 expression in airway epithelial cells (), peribronchial leukocytes (), and parenchymal leukocytes (). Conclusions. AE reduces smoke-induced COPD phenotype involving STAT3.