丙泊酚致学习记忆障碍下突触可塑性损害的机制研究进展  

Mechanistic advances in the impairment of synaptic plasticity under learning memory impairment caused by Propofol

作　　者：范舜钦 高宁[1] 王喜军 FAN Shunqin;GAO Ning;WANG Xijun(Department of Anesthesiology,Guangxi International Zhuang Medical Hospital Affiliated to Guangxi University of Traditional Chinese Medicine,Guangxi Zhuang Autonomous Region,Nanning530201,China)

机构地区：[1]广西中医药大学附属、广西国际壮医医院麻醉科,广西南宁530201

出　　处：《中国医药导报》2023年第28期45-48,53,共5页China Medical Herald

基　　金：广西壮族自治区中医药管理局科研基金项目(GXZYZ20210352);广西中医药大学研究生教育创新计划项目(YCSY2023059);广西国际壮医医院引进人才科研启动基金项目(GZ2021RC009)。

摘　　要：丙泊酚麻醉会引起大鼠的学习记忆障碍。其中涉及突触可塑性、氧化应激、细胞自噬及铁死亡等机制。突触可塑性的损害导致大鼠学习能力下降,无法形成长期记忆。恢复突触可塑性是逆转丙泊酚致学习记忆障碍的重要途径。近年来,表观遗传修饰、突触基因及相关蛋白的表达在促进突触可塑性的恢复,减轻神经元凋亡,促进学习记忆形成与巩固等方面发挥越来越重要的作用。本文就近年来上述机制促进突触可塑性的形成和维持,减轻丙泊酚导致的学习记忆障碍作一综述,以期为临床及基础研究减轻丙泊酚神经毒性作用提供理论依据。Propofol anesthesia can cause learning and memory impairment in rats.The mechanisms involved include synaptic plasticity,oxidative stress,autophagy,and iron death.Damage to synaptic plasticity leads to a reduced ability to learn and an inability to form long-term memories.Restoring synaptic plasticity is an important way to reverse Propofol induced learning and memory impairment.In recent years,epigenetic modifications,expression of synaptic genes and related proteins have played an increasingly important role in promoting the restoration of synaptic plasticity,alleviating neuronal apoptosis,and promoting the formation and consolidation of learning memories.In this paper,we review the above mechanisms to promote the formation and maintenance of synaptic plasticity and alleviate the learning memory impairment caused by Propofol in recent years,in order to provide a theoretical basis for clinical and basic research to alleviate the neurotoxic effects of Propofol.

关 键 词：突触可塑性 学习记忆 丙泊酚 表观遗传修饰 

分 类 号：R969[医药卫生—药理学]