运动抑制烟雾诱导的 COPD 涉及 STAT3 的调节。
Exercise Inhibits the Effects of Smoke-Induced COPD Involving Modulation of STAT3.
机构信息
Nove de Julho University, São Paulo, SP, Brazil.
Brazilian 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.
出版信息
Oxid Med Cell Longev. 2017;2017:6572714. doi: 10.1155/2017/6572714. Epub 2017 Oct 18.
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 ( < 0.001), lymphocytes ( < 0.001), and neutrophils ( < 0.001) in BAL, as well as BAL levels of IL-1 ( < 0.001), CXCL1 ( < 0.001), IL-17 ( < 0.001), and TNF- ( < 0.05), while increased the levels of IL-10 ( < 0.001). AE also inhibited smoke-induced increases in total leukocytes ( < 0.001), neutrophils ( < 0.05), lymphocytes ( < 0.001), and monocytes ( < 0.01) in blood, as well as serum levels of IL-1 ( < 0.01), CXCL1 ( < 0.01), IL-17 ( < 0.05), and TNF- ( < 0.01), while increased the levels of IL-10 ( < 0.001). AE reduced smoke-induced emphysema ( < 0.001) and collagen fiber accumulation in the airways ( < 0.001). AE reduced smoke-induced STAT3 and phospho-STAT3 expression in airway epithelial cells ( < 0.001), peribronchial leukocytes ( < 0.001), and parenchymal leukocytes ( < 0.001).
CONCLUSIONS
AE reduces smoke-induced COPD phenotype involving STAT3.
目的
评估 STAT3 在香烟诱导的 COPD 模型中有氧运动（AE）作用中的参与度。
方法
将雄性 C57Bl/6 小鼠分为对照组、运动组、COPD 组和 COPD+运动组。在 90 天期间给予香烟。从第 61 天开始至第 90 天进行跑步机有氧训练。评估肺部炎症、全身炎症、肺气肿程度和气道重塑。对气道上皮细胞、支气管周围白细胞和肺实质白细胞中 STAT3 的整体和磷酸化表达进行分析。
结果
AE 抑制了香烟诱导的 BAL 中总细胞（<0.001）、淋巴细胞（<0.001）和中性粒细胞（<0.001）的积聚，以及 BAL 中 IL-1（<0.001）、CXCL1（<0.001）、IL-17（<0.001）和 TNF-（<0.05）的水平，同时增加了 IL-10（<0.001）的水平。AE 还抑制了香烟诱导的血液中总白细胞（<0.001）、中性粒细胞（<0.05）、淋巴细胞（<0.001）和单核细胞（<0.01）、血清中 IL-1（<0.01）、CXCL1（<0.01）、IL-17（<0.05）和 TNF-（<0.01）的增加，同时增加了 IL-10（<0.001）的水平。AE 减少了香烟诱导的肺气肿（<0.001）和气道中胶原纤维的积累（<0.001）。AE 减少了香烟诱导的气道上皮细胞（<0.001）、支气管周围白细胞（<0.001）和肺实质白细胞（<0.001）中 STAT3 和磷酸化 STAT3 的表达。
结论
AE 减少了香烟诱导的 COPD 表型，涉及 STAT3。
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