PDF(Pubmed)
Abstract：
Ischemic stroke (IS) is one of the most fatal diseases. Neuroimmunity, inflammation, and oxidative stress play important roles in various complex mechanisms of IS. In particular, the early proinflammatory response resulting from the overactivation of resident microglia and the infiltration of circulating monocytes and macrophages in the brain after cerebral ischemia leads to secondary brain injury. Microglia are innate immune cells in the brain that constantly monitor the brain microenvironment under normal conditions. Once ischemia occurs, microglia are activated to produce dual effects of neurotoxicity and neuroprotection, and the balance of the two effects determines the fate of damaged neurons. The activation of microglia is defined as the classical activation (M1 type) or alternative activation (M2 type). M1 type microglia secrete pro-inflammatory cytokines and neurotoxic mediators to exacerbate neuronal damage, while M2 type microglia promote a repairing anti-inflammatory response. Fine regulation of M1/M2 microglial activation to minimize damage and maximize protection has important therapeutic value. This review focuses on the interaction between M1/M2 microglia and other immune cells involved in the regulation of IS phenotypic characteristics, and the mechanism of natural plant components regulating microglia after IS, providing novel candidate drugs for regulating microglial balance and IS drug development.
摘要：
缺血性卒中(IS)是最致命的疾病之一。神经免疫,炎症,氧化应激在IS的各种复杂机制中起着重要作用。特别是,脑缺血后脑中常驻小胶质细胞过度激活和循环单核细胞和巨噬细胞浸润引起的早期促炎反应导致继发性脑损伤。小胶质细胞是大脑中的先天免疫细胞，在正常条件下不断监测大脑微环境。一旦发生缺血,小胶质细胞被激活以产生神经毒性和神经保护的双重作用，两种效应的平衡决定了受损神经元的命运。小胶质细胞的激活被定义为经典激活(M1型)或替代激活(M2型)。M1型小胶质细胞分泌促炎细胞因子和神经毒性介质加剧神经元损伤，而M2型小胶质细胞促进修复抗炎反应。精细调控M1/M2小胶质细胞的激活使损伤最小化和保护最大化具有重要的治疗价值。本文就M1/M2小胶质细胞与其他免疫细胞之间的相互作用参与IS的表型特征进行综述,以及IS后天然植物成分调控小胶质细胞的机制，为调节小胶质细胞平衡和IS药物开发提供新的候选药物。
