国际麻醉学与复苏杂志   2013, Issue (2): 7-7
    
褪黑素与神经元退行性变和术后认知功能障碍
倪诚, 谭刚, 郭向阳1()
1.北京大学第三医院
The protective effects of melatonin on neural degenerative disease and postoperative cognitive dysfunction
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摘要:

背景 褪黑素易于穿越血脑屏障与中枢神经组织结合,外源性给予褪黑素通过抗氧化、抗炎症、抗细胞凋亡等多种作用,发挥神经保护作用。近年来的研究开始关注褪黑素对学习记忆、神经元退行性变、以及术后认知功能障碍(postoperative cognitive dysfunction, POCD)的影响以及作用机制。 目的 对褪黑素中枢神经系统保护作用的研究作一综述,为进一步研究褪黑素对中枢神经系统病变的作用,尤其是其在围术期的应用提供理论依据。 内容 介绍褪黑素对记忆、海马和其他脑区内长时程增强(long term potentiation, LTP)和突触形成过程的影响,并探讨相关机制,主要涉及褪黑素对神经传导系统的影响,对氧化应激、炎症、细胞凋亡等的抑制。阐述褪黑素对衰老和神经系统退行性疾病、多种因素所致POCD的保护作用。 趋向 学习记忆、衰老相关的认知功能障碍减退以及POCD的发生机制尚未完全清楚,但其中可能涉及共同的神经传导通路和病理学基础。褪黑素作为抗氧化剂和生物节律调节因子,拥有广泛的研究前景和临床应用价值。

关键词: 褪黑素; 脑保护; 记忆; 阿尔茨海默病; 术后认知功能障碍
Abstract:

Background Melatonin penetrates the blood-brain barrier and binds with brain neurons, and protects nervous system through antioxidant, anti-inflammation and anti-apoptosis effects. Recent studies have focused on the influence of exogenous melatonin on learning and memory, neural degenerative disease and postoperative cognitive dysfunction (POCD), and relevant mechanisms. Objective To provide basis for further investigation on protective effects of melatonin on central nervous system (CNS) pathology and perioperative application by reviewing recent investigations on neuroprotection of CNS. Content The influence of melatonin on memory, long term potentiation and neuronal plasticity in hippocampus and other brain regions, and underlying mechanisms including influence of neurotransmission system and inhibition of oxidative stress, inflammation and cellular apoptosis were introduced. The protective effects of melatonin on neurodegerative disease and POCD caused by multiple factors were discussed. Trend The mechanisms in learning and memory, cognitive dysfunction of the aged and POCD are still unclear, but the same neurotransmission pathway and pathology may be involved. As an antioxidant and circadian rhythm regulator, melatonin has wide prospects for investigation and values for clinical application.

Key words: Melatonin; Brain protection; Memory; Alzheimer′s disease; Postoperative cognitive dysfunction