We have located links that may give you full text access.
Exercise Inhibits the Effects of Smoke-Induced COPD Involving Modulation of STAT3.
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 ( p < 0.001), lymphocytes ( p < 0.001), and neutrophils ( p < 0.001) in BAL, as well as BAL levels of IL-1 β ( p < 0.001), CXCL1 ( p < 0.001), IL-17 ( p < 0.001), and TNF- α ( p < 0.05), while increased the levels of IL-10 ( p < 0.001). AE also inhibited smoke-induced increases in total leukocytes ( p < 0.001), neutrophils ( p < 0.05), lymphocytes ( p < 0.001), and monocytes ( p < 0.01) in blood, as well as serum levels of IL-1 β ( p < 0.01), CXCL1 ( p < 0.01), IL-17 ( p < 0.05), and TNF- α ( p < 0.01), while increased the levels of IL-10 ( p < 0.001). AE reduced smoke-induced emphysema ( p < 0.001) and collagen fiber accumulation in the airways ( p < 0.001). AE reduced smoke-induced STAT3 and phospho-STAT3 expression in airway epithelial cells ( p < 0.001), peribronchial leukocytes ( p < 0.001), and parenchymal leukocytes ( p < 0.001).
Conclusions: AE reduces smoke-induced COPD phenotype involving STAT3.
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 ( p < 0.001), lymphocytes ( p < 0.001), and neutrophils ( p < 0.001) in BAL, as well as BAL levels of IL-1 β ( p < 0.001), CXCL1 ( p < 0.001), IL-17 ( p < 0.001), and TNF- α ( p < 0.05), while increased the levels of IL-10 ( p < 0.001). AE also inhibited smoke-induced increases in total leukocytes ( p < 0.001), neutrophils ( p < 0.05), lymphocytes ( p < 0.001), and monocytes ( p < 0.01) in blood, as well as serum levels of IL-1 β ( p < 0.01), CXCL1 ( p < 0.01), IL-17 ( p < 0.05), and TNF- α ( p < 0.01), while increased the levels of IL-10 ( p < 0.001). AE reduced smoke-induced emphysema ( p < 0.001) and collagen fiber accumulation in the airways ( p < 0.001). AE reduced smoke-induced STAT3 and phospho-STAT3 expression in airway epithelial cells ( p < 0.001), peribronchial leukocytes ( p < 0.001), and parenchymal leukocytes ( p < 0.001).
Conclusions: AE reduces smoke-induced COPD phenotype involving STAT3.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app