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

Autor: Adriano Silva-Renno, Ana Paula Ligeiro de Oliveira, Manoel Carneiro Oliveira-Junior, Auriléia Aparecida de Brito, Asghar Abbasi, Alessandra Choqueta de Toledo-Arruda, André Luis Lacerda Bachi, Rodolfo de Paula Vieira, Maysa Alves Rodrigues Brandão-Rangel, Maria G. Belvisi
Jazyk: angličtina
Rok vydání: 2017
Předmět:
Male
0301 basic medicine
Aging
Neutrophils
Interleukin-1beta
Male mice
Lung pathology
Biochemistry
PATHWAY
Mice
Pulmonary Disease
Chronic Obstructive
0302 clinical medicine
Smoke
Lymphocytes
Phosphorylation
STAT3
Lung
COPD
ARREST
Physical conditioning
biology
lcsh:Cytology
Interleukin-17
General Medicine
CHEMOTAXIS
Interleukin-10
Pulmonary Emphysema
Cardiology
Airway Remodeling
AEROBIC EXERCISE
Life Sciences & Biomedicine
Bronchoalveolar Lavage Fluid
Research Article
STAT3 Transcription Factor
medicine.medical_specialty
Article Subject
Pulmonary disease
OBSTRUCTIVE PULMONARY-DISEASE
03 medical and health sciences
INFLAMMATION
Physical Conditioning
Animal
Internal medicine
medicine
Animals
Aerobic exercise
lcsh:QH573-671
Science & Technology
business.industry
Cell Biology
medicine.disease
Mice
Inbred C57BL
PHYSICAL-ACTIVITY
030104 developmental biology
030228 respiratory system
CIGARETTE-SMOKE
biology.protein
Physical therapy
ASTHMA
business
Zdroj: Oxidative Medicine and Cellular Longevity, Vol 2017 (2017)
Oxidative Medicine and Cellular Longevity
ISSN: 1942-0994
1942-0900
Popis: 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-1β (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-1β (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.
Databáze: OpenAIRE
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