吸入麻醉药促发育期神经元凋亡的分子机制  

The molecular mechanisms of inhalational anesthetics induced neuroapoptosis in the developing brain

作　　者：丁芳[1] 郑利民[2] 罗涛[2] 

机构地区：[1]安徽医科大学第二临床学院,合肥230032 [2]北京大学深圳医院麻醉科,518036

出　　处：《国际麻醉学与复苏杂志》2016年第2期184-188,共5页International Journal of Anesthesiology and Resuscitation

基　　金：国家自然科学基金（81271205）;深圳市卫计委临床技术研究及转化项目（201501025）

摘　　要：背景长期以来，人们一直认为吸入麻醉药的麻醉作用是可逆的，对中枢神经系统不会遗留任何副作用。近年基础研究发现，实验动物尤其是处于发育期动物，暴露于吸入麻醉药后，可出现记忆、认知功能障碍。这种现象的产生可能与吸入麻醉药导致的神经元凋亡增加有关。目的综述吸入麻醉药诱导发育期大脑神经元凋亡可能的分子机制。内容吸入麻醉药可能通过影响神经递质及受体、信号转导通路，并可引起氧化应激反应、p一淀粉样蛋白质集聚，从而导致神经细胞凋亡。趋向对吸入麻醉药神经毒性防治的研究起推动作用。Background The effect of inhaled anesthetics on central nervous system has long been considered to be reversible without any side effects. In recent years, the pre-clinical researches demonstrated that animals, particularly in the developmental stage, developed memory and cognitive dysfunction after exposure to inhaled anesthetics. The causes of this phenomenon may be related to inhalational anesthetics-induced neuronal apoptosis. Objective This review summarized the molecular mechanisms of neuroapoptosis in the developing brain induced by inhalational anesthetics. Content Inhalational anesthetics may facilitate neuroapoptosis through regulating neurotransmitters and their receptors, signal transduction pathways, oxidative stress, and β-amyloid protein accumulation. Trend These findings will help to improve the prevention or treatment of inhalational anesthetics-associated neurotoxicity.

关 键 词：吸入麻醉药 发育期 神经细胞 凋亡 分子机制 

分 类 号：R614[医药卫生—麻醉学]