缺血性脑卒中血脑屏障受损及修复的神经炎性机制研究进展

Research progress on neuroinflammatory mechanisms of blood-brain barrier damage and repair in ischemic stroke

缺血性脑卒中(ischemic stroke,IS)是目前威胁人类健康的重要疾病之一,IS的发生发展过程可触发一系列复杂的病理生理改变,包括血脑屏障受损、离子失衡、氧化应激、线粒体损伤等,最终导致缺血区神经细胞的凋亡及坏死。其中,血脑屏障受损是IS患者出现脑水肿、出血转化及预后不良的关键因素,而神经炎性反应在血脑屏障受损及修复过程中发挥重要作用。该文主要围绕胶质细胞、促炎性细胞因子及基质金属蛋白酶介导的神经炎性反应与IS血脑屏障受损及修复的相关机制进行综述,以期为IS的治疗提供新方向。

Ischemic stroke(IS) is one of the important diseases threatening human health. The occurrence and development of IS can trigger a series of complex pathophysiological changes, including damage to the blood-brain barrier, ion imbalance, oxidative stress, mitochondrial damage, which ultimately lead to the apoptosis and necrosis of nerve cells in the ischemic area. Impaired blood-brain barrier is a key factor for cerebral edema, hemorrhagic transformation and poor prognosis in patients with IS, and neuroinflammatory response plays an important role in the damage and repair of the blood-brain barrier. This article mainly focuses on the neuroinflammatory response mediated by glial cells, pro-inflammatory cytokines and matrix metalloproteinases and the related mechanisms of IS blood-brain barrier damage and repair, in order to provide new directions for the treatment of IS.