小胶质细胞在蛛网膜下腔出血后早期脑损伤中的作用和机制  

Role and mechanism of microglia in early brain injury after subarachnoid hemorrhage

作　　者：王萧逸 郑杰胜[1] 潘剑威[1] 詹仁雅[1] 周衡俊[1] Wang Xiaoyi;Zheng Jiesheng;Pan Jianwei;Zhan Renya;Zhou Hengjun(The First Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China)

机构地区：[1]浙江大学医学院附属第一医院,杭州310003

出　　处：《国际脑血管病杂志》2021年第7期549-554,共6页International Journal of Cerebrovascular Diseases

摘　　要：早期脑损伤(early brain injury,EBI)是指蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后72 h内、脑血管痉挛出现前发生的一系列病理生理学改变,是影响SAH转归的关键因素。其可能的病理机制包括细胞代谢、氧化应激及免疫炎症等,其中炎症反应发挥着重要作用。作为中枢神经系统的重要免疫细胞,小胶质细胞在脑损伤后发生M1/M2极化,一方面通过Toll样受体4(Toll-like receptor 4,TLR4)、钙敏感受体(calcium-sensing receptor,CaSR)和髓样细胞触发受体1(triggering receptor expressed on myeloid cells 1,TREM-1)等介导的信号通路分泌促炎性细胞因子,参与SAH后的神经元凋亡、血脑屏障破坏和脑水肿等过程,另一方面通过表达神经球蛋白和血红素加氧酶-1等发挥抗炎保护作用。文章就SAH后EBI中小胶质细胞的M1/M2极化过程及其双重作用机制进行了综述。Early brain injury(EBI)is a series of pathophysiological changes occurring within 72 h after subarachnoid hemorrhage(SAH)and before cerebral vasospasm,which is a key factor affecting the outcome of SAH.The possible pathological mechanisms include cell metabolism,oxidative stress and immune inflammation,in which inflammatory response plays an important role.As the important immune cells in the central nervous system,microglia undergo M1/M2 polarization after brain injury.On the one hand,microglia secrete proinflammatory cytokines through Toll-like receptor 4(TLR4),calcium sensing receptor(CaSR)and triggering receptor expressed on myoid cells 1(TREM-1)mediated signaling pathways,which are involved in neuronal apoptosis,blood-brain barrier damage and brain edema after SAH.On the other hand,microglia play the anti-inflammatory and protective effects through the expression of neuroglobin and heme oxygenase 1.This article reviews the M1/M2 polarization process of microglia in EBI after SAH and its dual mechanisms of action.

关 键 词：蛛网膜下腔出血 脑损伤 小胶质细胞 炎症 细胞凋亡 血脑屏障 脑水肿 神经保护 

分 类 号：R743.35[医药卫生—神经病学与精神病学]