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氧化应激在慢性阻塞性肺疾病中的作用。

The role of oxidative stress in chronic obstructive pulmonary disease.

作者信息

Bowler Russell P, Barnes Peter J, Crapo James D

机构信息

Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado 80206, USA.

出版信息

COPD. 2004;1(2):255-77. doi: 10.1081/copd-200027031.

Abstract

Tobacco smoke is the number one risk factor for chronic obstructive pulmonary disease (COPD) and contains a high concentration of oxidants. The lung has a high concentration of antioxidants and antioxidant enzymes; however, COPD patients show evidence of increased oxidative stress suggesting that endogenous antioxidants may be insufficient to prevent oxidative damage from cigarette smoke. The consequences of increased oxidative stress in the lung include increased transcription of inflammatory genes, increased protease activity, and increased mucus secretion. Oxidative stress is often associated with impaired skeletal muscle function and may be one of the causes of glucocorticoid resistance. While current pharmacologic approaches to the treatment of chronic obstructive pulmonary disease do not commonly include antioxidants, preclinical studies involving animal models suggest that antioxidant superoxide dismutase mimetics offer a potential new therapeutic approach to the prevention and treatment of chronic obstructive pulmonary disease.

摘要

烟草烟雾是慢性阻塞性肺疾病(COPD)的首要危险因素,且含有高浓度的氧化剂。肺中含有高浓度的抗氧化剂和抗氧化酶;然而,COPD患者有氧化应激增加的迹象,这表明内源性抗氧化剂可能不足以防止香烟烟雾造成的氧化损伤。肺中氧化应激增加的后果包括炎症基因转录增加、蛋白酶活性增加和黏液分泌增加。氧化应激常与骨骼肌功能受损相关,可能是糖皮质激素抵抗的原因之一。虽然目前治疗慢性阻塞性肺疾病的药物方法通常不包括抗氧化剂,但涉及动物模型的临床前研究表明,抗氧化超氧化物歧化酶模拟物为预防和治疗慢性阻塞性肺疾病提供了一种潜在的新治疗方法。

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