内质网应激在全身麻醉诱导神经毒性中的作用及机制研究进展  

Research Progress in Role and Mechanism of Endoplasmic Reticulum Stress in Neurotoxicity Induced by General Anesthesia

作　　者：魏路 黄磊[1] 孟庆涛[1] WEI Lu;HUANG Lei;MENG Qingtao(Department of Anesthesiology,Renmin Hospital of Wuhan University,Wuhan 430060,China)

机构地区：[1]武汉大学人民医院麻醉科,武汉430060

出　　处：《医学综述》2023年第23期5228-5232,5239,共6页Medical Recapitulate

摘　　要：全身麻醉相关神经毒性的机制是麻醉科、外科等众多学科的重点研究方向,而内质网应激(ERS)是全身麻醉诱导神经毒性的关键环节。ERS通过激活肌醇需求酶1α、蛋白激酶RNA样内质网激酶、激活转录因子6信号通路,以不同方式诱导神经细胞凋亡,从而导致全身麻醉相关神经毒性。全身麻醉虽然能够减少炎症和氧化反应,但也能够通过激活ERS的途径诱发炎症反应和氧化应激,炎症和氧化应激分别通过抑制抗凋亡因子生成、损伤细胞线粒体等方式促进神经细胞凋亡,从而导致神经损害。未来在预防全身麻醉相关神经毒性中,通过干预ERS相关信号通路,有助于减少炎症和氧化应激,降低麻醉药物对神经功能的损伤。The mechanism of neurotoxicity related to general anesthesia is the key research direction of many disciplines such as anesthesiology and surgery,and endoplasmic reticulum stress(ERS)is the key link of neurotoxicity induced by general anesthesia.ERS induces neuronal apoptosis in different ways of activation of inositol-requiring enzyme 1α,protein kinase RNA-like endoplasmic reticulum kinase,and activating transcription factor 6 signaling pathways,leading to neurotoxicity associated with general anesthesia.Although general anesthesia can reduce inflammation and oxidative reaction,it can also induce inflammation and oxidative stress by activating ERS.Inflammation and oxidative stress promote nerve cell apoptosis by inhibiting the production of anti-apoptotic factors and damaging cell mitochondria,respectively,resulting in neurological damage.In the future,in the prevention of general anesthesia related neurotoxicity,intervening in the ERS related signaling pathway can help reduce inflammation and oxidative stress,and reduce the damage of anesthesia drugs to neurological function.

关 键 词：全身麻醉 神经毒性 内质网应激 炎症反应 氧化应激 

分 类 号：R614.2[医药卫生—麻醉学]