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暴露于环境细颗粒物导致大鼠模型中 COPD 的发生及其潜在机制的描述。

Exposure to Ambient Particulate Matter Induced COPD in a Rat Model and a Description of the Underlying Mechanism.

机构信息

The State Key Lab of Respiratory Disease, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.

The School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.

出版信息

Sci Rep. 2017 Mar 31;7:45666. doi: 10.1038/srep45666.

DOI:10.1038/srep45666
PMID:28361885
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5374504/
Abstract

While the health effects of air pollution have been an international public health concern since at least the 1950s, recent research has focused on two broad sources of air pollution, namely, biomass fuel (BMF) and motor vehicle exhaust (MVE). Many studies have shown associations between air pollution PM and exacerbations of pre-existing COPD, but the role of air pollution PM in the development and progression of COPD is still uncertain. The current study indicates that rats can develop pronounced COPD following chronic exposure to air pollution PM (BMF and MVE), as characterized by lung function reduction, mucus metaplasia, lung and systemic inflammation, emphysema, and small airway remodeling. Comparative analyses demonstrate that both BMF and MVE activate similar pathogenesis that are linked to the development of COPD. These findings also show that some differences are found in the lungs of rats exposed to BMF or MVE, which might result in different phenotypes of COPD.

摘要

尽管空气污染对健康的影响至少从 20 世纪 50 年代以来一直是国际公共卫生关注的问题,但最近的研究集中在空气污染的两个主要来源,即生物量燃料(BMF)和汽车尾气(MVE)。许多研究表明,空气污染 PM 与 COPD 的恶化之间存在关联,但空气污染 PM 在 COPD 的发展和进展中的作用仍不确定。本研究表明,大鼠在慢性暴露于空气污染 PM(BMF 和 MVE)后可发展为明显的 COPD,其特征是肺功能下降、粘液化生、肺和全身炎症、肺气肿和小气道重塑。比较分析表明,BMF 和 MVE 都激活了类似的发病机制,这些机制与 COPD 的发展有关。这些发现还表明,暴露于 BMF 或 MVE 的大鼠肺部存在一些差异,这可能导致 COPD 的不同表型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9c4/5374504/f2d2e81edfae/srep45666-f8.jpg
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