摘要
氧化/抗氧化失衡导致的氧化应激是慢性阻塞性肺疾病（COPD）重要发病机制之一。许多研究发现在COPD患者和吸烟的气道、呼出气、血液和尿中都有氧化应激标志物水平的明显增高。氧化应激会直接损伤气道上皮,能够使抗蛋白水解酶失活,加重肺部微血管中中性粒细胞的聚集,激活氧化还原敏感的转录因子如核因子-κB和激活蛋白-1而使致炎因子基因的表达增加,加剧COPD患者肺部的炎症反应。COPD患者中的氧化负荷主要来源于香烟烟雾中的氧化物、气道和血液中白细胞释放活性氧物质（ROS）的增多和大气污染。氧化应激和抗氧化物的不足有关,补充抗氧化物可能会减轻氧化应激,所以在COPD的治疗中使用有较好生物活性的抗氧化物或具有抗氧化酶活性的物质可能会减轻氧化应激,最终减轻炎症反应。本文就氧化应激在COPD发病中的作用、抗氧化治疗在COPD治疗中的作用等方面的研究进展作一综述。
Oxidative stress which results from an oxidant/antioxidant imbalance is thought to play an important part in the pathogenesis of COPD. A number of studies have shown increased markers of oxidative stress in the airspaces, breath, blood, and urine in the patients with COPD. In the pathogenesis of COPD, oxidative stress may cause directly airspace epithelial injury, oxidative inactivation of antiproteinases, increased sequestration of neutrophils in the pulmonary microvasculature, and activation of redox-sensitive transcriptions factors such as nuclear factor-κB and activator protein-1 which increase the gene expression of proinflammatory mediators. The sources of the increased oxidative stress in the patients with COPD are derived from the increased burden of oxidants present in cigarette smoke, or from the increased amounts of reactive oxygen species released from leukocytes, both in the airspaces and in the blood, or from the air pollution. Antioxidant depletion or deficiency in antioxidants may contribute to oxidative stress. So dietary supplementation of antioxidants that have good bioavailability or molecules that have antioxidant enzyme activity may be therapies that not only protect against the attack of oxidants, but may fundamentally alter the inflammatory events. This article reviews the presently available experimental and clinical data on the role of oxidative stress in the pathogenesis of COPD, and the application of antioxidants in the treatment of this disease.
出处
《国际呼吸杂志》
2007年第9期692-695,共4页
International Journal of Respiration
关键词
慢性阻塞性肺疾病
氧化应激
抗氧化物
Chronic obstructive pulmonary disease
Oxidative stress
Antioxidant
