神经炎症在动脉瘤性蛛网膜下腔出血后早期脑损伤中的作用  

The Role of Neuroinflammation in Early Brain Injury after Aneurysmal Subarachnoid Hemorrhage

作　　者：廖艺斐 张慧 邹良玉[1] LIAO Yi-Fei;ZHANG Hui;ZOU Liang-Yu(Department of Neurology,The Second Clinical School of Jinan University,The First Affiliated Hospital of South University of Science and Technology,Shenzhen People's Hospital,Shenzhen 518000,China)

机构地区：[1]暨南大学第二临床医学院/南方科技大学第一附属医院/深圳市人民医院神经内科,深圳518000

出　　处：《中国卒中杂志》2021年第1期92-96,共5页Chinese Journal of Stroke

基　　金：广东省重点领域研发计划(2018B030336001)。

摘　　要：早期脑损伤(early brain injury,EBI)是影响动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage,aSAH)患者预后的重要因素之一。目前aSAH后EBI产生机制尚不明确,神经炎症可能为其主要驱动因素,其作用机制包括:红细胞降解产物和激活的小胶质细胞诱导神经炎症促进神经元凋亡;神经炎症通过激活星形胶质细胞破坏血脑屏障导致脑水肿,并募集外周中性粒细胞黏附于颅内微脉管系统引起微血管功能障碍导致脑皮质灌注不足。应用针对神经炎症不同靶点的药物预防EBI可能是当前治疗aSAH的新方向。Early brain injury(EBI)is one of the important factors affecting the prognosis of patients with aneurysmal subarachnoid hemorrhage(aSAH).At present,the mechanism of EBI after aSAH is not clear,and neuroinflammation may be the main driving factor.Its mechanism includes that red blood cell degradation products and activated microglia induce neuroinflammation and promote neuronal apoptosis;neuroinflammation activates astrocytes to destroy the blood-brain barrier,leading to brain edema,and recruits peripheral neutrophils to adhere to the intracranial microvasculature,causing microvascular dysfunction,and leading to insufficient cerebral cortex perfusion.The novel drugs targeted at neuroinflammation to prevent EBI may be a new direction for the current treatment of aSAH.

关 键 词：动脉瘤性蛛网膜下腔出血 早期脑损伤 神经炎症 

分 类 号：R743.35[医药卫生—神经病学与精神病学] R651.15[医药卫生—临床医学]