神经炎症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 neuroinflammation in early brain injury after subarachnoid hemorrhage

蛛网膜下腔出血(subarachnoid hemorrhage,SAH)的病理生理学机制主要包括早期脑损伤(early brain injury,EBI)和迟发性脑缺血。近年来的研究主要集中在EBI方面。血液进入蛛网膜下腔后会导致神经元凋亡、血脑屏障破坏、脑水肿和神经炎症,红细胞及其代谢产物会激活中枢神经系统驻留免疫细胞并招募外周炎症细胞浸润至蛛网膜下腔,诱导神经炎症。神经炎症在EBI中发挥着重要作用,对蛛网膜下腔出血患者的转归产生极大影响。文章对神经炎症在SAH后EBI中的作用进行了综述。

The pathophysiological mechanisms of subarachnoid hemorrhage(SAH)include early brain injury(EBI)and delayed cerebral ischemia.In recent years,researches have mainly focused on EBI.After blood enters the subarachnoid space,it can cause neuronal apoptosis,blood-brain barrier disruption,brain edema and neuroinflammation.Red blood cells and their metabolites activate resident immune cells in central nervous system and recruit peripheral inflammatory cells tinto the subarachnoid space,inducing neuroinflammation.The latter plays an important role in EBI and has a significant impact on the outcome of patients with SAH.This article reviews the role of neuroinflammation in EBI after SAH.