期刊
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
卷 256, 期 -, 页码 97-108出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.resp.2017.04.010
关键词
Sleep apnea; Obstructive; Hypoxia; Intermittent; Fibrosis; Lung/immunology/metabolism/pathology
资金
- Department of Medicine, University of Wisconsin School of Medicine and Public Health
- NIH-NHLBI R01 Supplement [HL1150613]
- [NIH-NHLBI R01 - HL115061]
Obstructive sleep apnea (OSA) has been linked to increased mortality in pulmonary fibrosis. Its key feature, chronic intermittent hypoxia (CIH), can lead to oxidative stress and inflammation, known to lead to fibrotic pathology in other organs. We tested the effects of CIH in an animal model of bleomycin-induced lung fibrosis. Sprague Dawley rats were instilled intratracheally with bleomycin (Blm) or saline (Sal), and exposed to CIH or normal air (Norm) for 9 or 30 days. Pulmonary function was tested and lungs were harvested for histological and molecular analyses. In Blm-treated animals, 30 days of CIH compared to Norm increased total lung collagen content (p = 0.008) and reduced Quasi-static lung compliance (p = 0.04). CIH upregulated lipid peroxidation and increased NF-x13 activation, IL-17 mRNA and Collal mRNA expression. Our results indicate that following Blm-induced lung injury, CIH amplifies collagen deposition via oxidative and inflammatory pathways, culminating in stiffer lungs. Thus, OSA may augment fibrosis in patients with interstitial lung disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据