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

Autor(es)

Rodrigues Brandao-Rangel, Maysa Alves ^{[1, 2]} ; Lacerda Bachi, Andre Luis ^[3] ; Oliveira-Junior, Manoel Carneiro ^{[1, 2]} ; Abbasi, Asghar ^[4] ; Silva-Renno, Adriano ^{[1, 2]} ; de Brito, Aurileia Aparecida ^[1] ; Ligeiro de Oliveira, Ana Paula ^[1] ; Toledo-Arruda, Alessandra Choqueta ^[5] ; Belvisi, Maria Gabriela ^[6] ; Vieira, Rodolfo Paula ^{[1, 2]}

Afiliação do(s) autor(es)

^[1] Nove de Julho Univ, Sao Paulo, SP - Brazil

^[2] Sao Jose dos Campos Humanitas & Univ Brasil, Sch Med Sci, Brazilian Inst Teaching & Res Pulm & Exercise Imm, Sao Paulo, SP - Brazil

^[3] Cruzeiro do Sul Univ, Inst Phys Act Sci & Sports, Postgrad Program Human Movement Sci, Sao Paulo, SP - Brazil

^[4] Univ Calif Irvine, Inst Memory Impairments & Neurol Disorders, MIND Inst, Irvine, CA - USA

^[5] Univ Sao Paulo, Sch Med, Dept Med, Lab Expt Therapeut LIM 20, Sao Paulo, SP - Brazil

^[6] Imperial Coll London, Natl Heart & Lung Inst, Resp Pharmacol Grp, Airway Dis, London - England

• Tipo de documento: Artigo Científico
• Fonte: OXIDATIVE MEDICINE AND CELLULAR LONGEVITY; 2017.
• Citações Web of Science: 4

Resumo

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 beta (p < 0 001), CXCL1 (p < 0 001), IL-17 (p < 0 001), and TNF-alpha (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 beta (p < 0 01), CXCL1 (p < 0 01), IL-17 (p < 0 05), and TNF-a (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. (AU)

• Processo FAPESP: 16/50010-0 - Involvement of socs-jak-stat signalling in the effects of aerobic exercise in a model of asthma
• Beneficiário: Rodolfo de Paula Vieira
• Linha de fomento: Auxílio à Pesquisa - Regular
• Processo FAPESP: 14/14604-8 - Papel da sinalização purinérgica nos efeitos anti-inflamatórios do treinamento aeróbio em um modelo de asma induzida por ácaro de poeira doméstica
• Beneficiário: Manoel Carneiro de Oliveira Junior
• Linha de fomento: Bolsas no Brasil - Doutorado
• Processo FAPESP: 12/15165-2 - Papel da sinalização purinérgica e da sinalização SOCS-JAK-STAT nos efeitos antiinflamatórios do treinamento aeróbio em modelos experimentais de asma e em indivíduos asmáticos
• Beneficiário: Rodolfo de Paula Vieira
• Linha de fomento: Auxílio à Pesquisa - Apoio a Jovens Pesquisadores