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阻塞性睡眠呼吸暂停、氧化应激、炎症和内皮功能障碍——预测性实验室生物标志物概述。

Obstructive Sleep Apnea, oxidative stress, inflammation and endothelial dysfunction-An overview of predictive laboratory biomarkers.

机构信息

Department of Surgical Sciences, Molecular Biology Service (MBS), University of Cagliari, Cagliari, Italy.

出版信息

Eur Rev Med Pharmacol Sci. 2020 Jun;24(12):6939-6948. doi: 10.26355/eurrev_202006_21685.

Abstract

OBJECTIVE

Obstructive Sleep Apnea (OSA) represents an emerging public health concern with great impact on cardiovascular state. Oxidative stress (OS), inflammation and altered Nitric Oxide (NO) production are recognized as prominent mechanisms of many acute and chronic diseases and even of the normal aging process. They are investigated as major pathophysiological processes in OSA through the analysis and comparison of significative and validated biomarkers.

MATERIALS AND METHODS

The review is developed using as key terms "sleep apnea", "oxidative stress", "inflammation", and "endothelial dysfunction". Included studies must have followed the American Academy of Sleep Medicine guidelines according to the diagnosis and classification of OSA. Lipid, protein and DNA oxidation products, PCR, IL-6, IL-8, TNF-α, NO and nitrosative stress compounds, and endothelial functioning tests have been detected for their contribution in OSA along the last 3 decades.

RESULTS

Nocturnal intermittent hypoxia has emerged to be significantly associated to oxidative/nitrosative stress, increase in pro-inflammatory markers, imbalance in NO production, and endothelium impairment. Body Mass Index (BMI) contribution needs further clarifications. Continuous Positive Airway Pressure (CPAP) therapy has demonstrated beneficial effects on vascular function and pro-inflammatory milieu in OSA.

CONCLUSIONS

Oxidative stress and Inflammation significantly correlate with OSA; similarly, vascular functioning is impaired in accordance to unregulated levels of NO and derived compounds. Continuous Positive Airway Pressure markedly improves oxidative stress, inflammation and endothelial dysfunction in OSA.

摘要

目的

阻塞性睡眠呼吸暂停(OSA)是一个新兴的公共卫生关注点,对心血管状况有重大影响。氧化应激(OS)、炎症和一氧化氮(NO)产生的改变被认为是许多急性和慢性疾病甚至正常衰老过程的主要机制。通过分析和比较有意义和经过验证的生物标志物,这些机制被认为是 OSA 的主要病理生理过程。

材料和方法

本综述使用“睡眠呼吸暂停”、“氧化应激”、“炎症”和“内皮功能障碍”作为关键词进行开发。纳入的研究必须根据美国睡眠医学学会的指南,根据 OSA 的诊断和分类进行。脂质、蛋白质和 DNA 氧化产物、PCR、IL-6、IL-8、TNF-α、NO 和硝化应激化合物以及内皮功能测试已被检测到,以了解它们在过去 30 年中对 OSA 的贡献。

结果

夜间间歇性低氧与氧化/硝化应激、促炎标志物增加、NO 产生失衡和内皮损伤显著相关。体重指数(BMI)的贡献需要进一步澄清。持续气道正压通气(CPAP)治疗已证明对 OSA 患者的血管功能和促炎环境具有有益影响。

结论

氧化应激和炎症与 OSA 显著相关;同样,NO 和衍生化合物的调节水平也会损害血管功能。持续气道正压通气(CPAP)显著改善 OSA 中的氧化应激、炎症和内皮功能障碍。

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