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氧化应激是慢性阻塞性肺疾病发病机制的核心吗?

Is oxidative stress central to the pathogenesis of chronic obstructive pulmonary disease?

作者信息

MacNee W, Rahman I

机构信息

Respiratory Medicine, ELEGI, Colt Research Laboratories, Wilkie Building, Medical School, Teviot Place, EH8 9AG, Edinburgh, UK.

出版信息

Trends Mol Med. 2001 Feb;7(2):55-62. doi: 10.1016/s1471-4914(01)01912-8.

DOI:10.1016/s1471-4914(01)01912-8
PMID:11286755
Abstract

There is now considerable evidence for an increased oxidant burden in patients with chronic obstructive pulmonary disease (COPD). Oxidative stress is a critical feature in the pathogenesis of COPD, since it results in inactivation of antiproteinases, airspace epithelial injury, MUCUS HYPERSECRETION, increased influx of neutrophils into the lungs, transcription factor activation and gene expression of pro-inflammatory mediators. Antioxidants should therefore not only protect against the direct injurious effects of oxidants, but also may fundamentally alter the inflammatory events which have a central role in the pathogenesis of COPD.

摘要

目前有大量证据表明,慢性阻塞性肺疾病(COPD)患者的氧化剂负荷增加。氧化应激是COPD发病机制中的一个关键特征,因为它会导致抗蛋白酶失活、肺泡上皮损伤、黏液分泌过多、中性粒细胞向肺部的流入增加、转录因子激活以及促炎介质的基因表达。因此,抗氧化剂不仅应能保护机体免受氧化剂的直接损伤作用,还可能从根本上改变在COPD发病机制中起核心作用的炎症事件。

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