Exercise inhibits the effects of smoke-induced COPD involving modulation of STAT3
File(s)
Author(s)
Rodrigues Brandao-Rangel, Maysa Alves
Lacerda Bachi, Andre Luis
Oliveira-Junior, Manoel Carneiro
Abbasi, Asghar
Silva-Renno, Adriano
Type
Journal Article
Abstract
Purpose
. Evaluate the participation of STAT3 in the e
ff
ects 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 in
fl
ammation, systemic in
fl
ammation, 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
fi
ber 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.
. Evaluate the participation of STAT3 in the e
ff
ects 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 in
fl
ammation, systemic in
fl
ammation, 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
fi
ber 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.
Date Issued
2017-10-18
Date Acceptance
2017-08-29
Citation
Oxidative Medicine and Cellular Longevity, 2017, 2017
ISSN
1942-0900
Publisher
Hindawi Publishing Corporation
Journal / Book Title
Oxidative Medicine and Cellular Longevity
Volume
2017
Copyright Statement
© 2017 Maysa Alves Rodrigues Brandao-Rangel et al. This is an open access article distributed under the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Identifier
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000413153200001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
Subjects
Science & Technology
Life Sciences & Biomedicine
Cell Biology
OBSTRUCTIVE PULMONARY-DISEASE
AEROBIC EXERCISE
PHYSICAL-ACTIVITY
CIGARETTE-SMOKE
INFLAMMATION
LUNG
CHEMOTAXIS
PATHWAY
ARREST
ASTHMA
Publication Status
Published
Article Number
ARTN 6572714