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瘦素作为抗氧化剂在阻塞性睡眠呼吸暂停中的作用:一项使用电子顺磁共振法的体外研究。

Role of leptin as antioxidant in obstructive sleep apnea: an in vitro study using electron paramagnetic resonance method.

机构信息

University of Virginia School of Medicine, Charlottesville, VA, USA.

出版信息

Sleep Breath. 2013 Mar;17(1):105-10. doi: 10.1007/s11325-012-0656-8. Epub 2012 Feb 4.

Abstract

INTRODUCTION

As in obstructive sleep apnea (OSA), the chronic cycles of hypoxia and reoxygenation are thought to be conducive of oxidative stress (OS) with generation of reactive oxygen species, identifying effective mechanisms of protection against oxidant-mediated tissue damage becomes of outmost importance. Leptin's role had been recently extended into that of participant to OS; while its exact role in this process is yet to be defined, elevated leptin levels correlate significantly with several indices of OSA disease severity such as nocturnal hypoxemia, possibly acting as a counteractive mechanism against the chronic intermittent hypoxia-related OS and serving as a marker of future risk of atherosclerotic disease. We therefore investigated leptin's antioxidant mechanism on superoxide (O (2) (-•) ) anions using spectrophotometry and electron paramagnetic resonance (EPR).

METHODS

The O (2) (-•) was generated by oxidation of xanthine (XAN) by xanthine oxidase (XO) in the presence of spin trap 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide with various concentrations of leptin (0.001, 0.01, 0.1, and 1 mg/ml) and without leptin. Signal intensity between 3,440 and 3,540 G was expressed as standard means ± SD. The activity of leptin on XO was determined by monitoring the conversion of XAN to uric acid at 293 nm using a Beckman DU 800 UV-visible spectrophotometer.

RESULTS

Leptin added to aqueous solutions at 0.1 and 1 mg/ml concentrations was associated with a statistically significant decrease in the EPR signal due to leptin's direct scavenging activity towards the O (2) (-•) .

CONCLUSION

Leptin is an antioxidant agent of possible use as a marker of OS and future risk of atherosclerotic disease in OSA.

摘要

简介

与阻塞性睡眠呼吸暂停(OSA)一样,人们认为慢性缺氧和再氧化循环有利于氧化应激(OS),从而产生活性氧(ROS),因此,寻找有效的抗氧化机制来防止氧化剂介导的组织损伤变得至关重要。瘦素的作用最近扩展到参与 OS;虽然其在该过程中的确切作用尚未确定,但升高的瘦素水平与 OSA 疾病严重程度的几个指数显著相关,例如夜间低氧血症,可能作为对抗与慢性间歇性低氧相关的 OS 的拮抗机制,并作为未来发生动脉粥样硬化疾病风险的标志物。因此,我们使用分光光度法和电子顺磁共振(EPR)研究了瘦素对超氧阴离子(O 2 (-•) )的抗氧化机制。

方法

在黄嘌呤氧化酶(XO)存在下,黄嘌呤(XAN)氧化生成 O 2 (-•) ,并用不同浓度的瘦素(0.001、0.01、0.1 和 1 mg/ml)和不含瘦素处理自旋捕获 5-二乙氧基磷酰基-5-甲基-1-吡咯啉 N-氧化物。3440 和 3540 G 之间的信号强度表示为标准均值±SD。通过在 293 nm 处监测 XAN 转化为尿酸来确定瘦素对 XO 的活性,使用贝克曼 DU 800 UV-可见分光光度计。

结果

在 0.1 和 1 mg/ml 浓度下添加到水溶液中的瘦素与 EPR 信号的统计学显著降低有关,这是由于瘦素对 O 2 (-•) 的直接清除活性。

结论

瘦素是 OS 的抗氧化剂,可能用作 OSA 中 OS 和未来发生动脉粥样硬化疾病的标志物。

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