小胶质细胞参与间歇低氧对中枢神经系统神经元的损伤

Intermittent hypoxia may cause neuronal impairment in central nervous system and the potential role played by microglia

阻塞性睡眠呼吸暂停（obstructivesleepapnea，OsA）是一种以睡眠期间上气道反复发生完全（呼吸暂停）或部分（低通气）阻塞导致低氧血症和夜间反复觉醒为特征的常见慢性疾病。0SA所造成的间歇低氧（IH）可导致中枢神经系统（CNS）结构性神经元损伤与功能障碍，在临床上表现为神经认知与行为障碍，其主要病生理基础在细胞水平上可被归为小胶质细胞为主的氧化应激和炎性损伤。小胶质细胞是CNS中主要的炎症细胞，通过线粒体、NADPH氧化酶以及兴奋性神经毒性递质的释放来引发CNs氧化应激和炎症。小胶质细胞为主的炎症过程是把双刃剑，神经毒性与神经保护之间、炎症与抗炎小胶质细胞细胞因子之间的平衡决定了小胶质细胞在OSAIH暴露后最终扮演的角色。小胶质细胞炎性损伤一旦启动，可能会持续不停并级联放大，最终导致有临床意义的CNs神经元损伤。本文将综述OSAIH对CNS结构性神经元的损伤极其并发的功能障碍，以及在小胶质细胞可能发挥的作用及其可能机制。

Obstructive sleep apnea （OSA） is a common condition characterized by repetitive episodes of complete （apnea） or partial （hypopnea） obstruction of the upper airway during sleep, resulting in oxygen desaturation and arousal from sleep. Intermittent hypoxia （IH） resulted from OSA may cause structural neuron damages and dysfunction in central nervous system （CNS）. Clinically, it manifests neurocognitive and behavioral deficits with oxidative stress and inflammatory impairment as its pathophysiological basis which are mediated by mieroglia at cellular level. Mieroglia are dominant pro- inflammatory cells in CNS. They induced CNS oxidative stress and inflammation mainly through mitochondria,reduced nicotinamide adenine dinucleotide phosphate （NADPH） oxidase, and the release of excitatory toxic neurotransmitter. The halanee between neurotoxic versus protective and anti-versus pro- inflammatory microglial factors might determine the final role of microglia after IH exposure from OSA. Microglia inflammatory impairment will be continuous and cascade upon activation, ultimately result in clinically significant neuron damages in CNS. In this review article,we will summarize the mechanisms of structural neuron damages in CNS and their concomitant dysfunction from IH of OSA, and the potential roles played by microglia in this process also will be described.