缺血性脑卒中免疫炎症反应机制的研究进展

Research progress of immune-inflammatory response mechanisms in ischemic stroke

缺血性脑卒中(ischemic stroke,IS)是世界范围内引起人类死亡、残疾的重大疾病。卒中早期,由死亡和受损神经元释放的多种损伤相关模式分子诱导神经胶质活化、外周免疫应答以及炎性介质分泌增加,从而加速血脑屏障破坏、加剧脑水肿和微循环障碍,造成继发性脑损伤。急性期后,免疫细胞逐渐通过表型改变促进神经元修复,再加上卒中诱导的免疫抑制作用共同影响着卒中的最终结局。本文就炎症反应及免疫应答在缺血性脑卒中发展中的作用机制进行综述,为靶向炎症损伤的缺血性脑卒中辅助治疗药物研发提供参考。

Ischemic stroke is a major disease that causes human death and disability in worldwide.In the early stage of ischemic stroke,danger-/damage-associated molecular patterns(DAMPs)released by injured and dying neurons can induce microglial activation,peripheral immune cell response and increase of inflammatory mediators.This local inflammation leads to the destruction of blood-brain barrier,brain edema and microcirculation disorder,which aggravates secondary brain injury.After the acute phase,various immune cells gradually promote neuronal repairment through phenotypic changes.Combined with stroke induced immunodepression phenomenon,these factors jointly affect the final outcome of stroke.This article reviews the mechanisms of inflammatory response and immune response in the development of ischemic stroke,and provides reference for further researches and development of adjuvant therapy drugs targeting inflammatory injury in ischemic stroke.