小胶质细胞极化及重编程在脑缺血再灌注损伤中的研究进展OA
Research advances on microglia polarization and reprogramming in cerebral ischemia-reperfusion injury
小胶质细胞(MG)是脑组织中重要的、固有先天性免疫细胞,可发挥吞噬病原体、杀伤靶细胞、抗原提呈、免疫调节、抗炎修复、促进神经元存活等功能.脑缺血再灌注损伤(CIRI)是继发于缺血性脑卒中后血管血流再通引起的严重脑血管疾病.在CIRI早期,过度激活的M1型MG可导致炎症风暴和血脑屏障破坏等损伤,而后期M2型极化对于组织抗炎、功能修复则起着至关重要的作用.但MG及其重编程在CIRI中的相关干预治疗机制尚未明确.本文综述基于MG表型调控的CIRI潜在治疗策略,即MG通过吞噬功能及抗炎修复作用参与缓解CIRI;通过代谢重编程及极化为M2表型后,其抗炎、抗氧化应激及促再生能力显著增强;通过清除细胞碎片、抑制神经炎症及促进组织重塑改善预后,以期为MG治疗CIRI的深入研究提供参考.
Microglia(MG)is an important and inherently innate immune cell in brain tissue.It can play the roles of phagocytosis of pathogens,killing of target cells,antigen presentation,immunomodulation,anti-inflammatory repair,and promotion of neuronal survival,etc.Cerebral ischemia-reperfusion injury(CIRI)is a severe cerebrovascular disease caused by vascular blood flow recanalization secondary to ischemic stroke.In the early stage of CIRI,over-activated M1-type MGs lead to injuries such as inflammatory storm and blood-brain barrier disruption,and in the later stage,M2-type polarization plays a crucial role in anti-inflammatory and functional repair of tissues.However,the interventional therapeutic mechanisms associated with MG and its reprogramming in CIRI have not been clarified.The aim of this paper is to review the potential therapeutic strategies of CIRI based on MG phenotypic regulation,i.e.,MG is involved in alleviating CIRI through phagocytosis and anti-inflammatory and repairing effects,and its anti-inflammatory,anti-oxidative stress,and pro-regenerative abilities are significantly enhanced by metabolic reprogramming and polarization to M2 phenotype,which improves the prognosis by removing cellular debris,inhibiting neuroinflammation,and promoting tissue remodeling,and provides a reference for the in-depth research on MG therapy for CIRI.
李雪莲;白文娅;邵建林
昆明医科大学麻醉学院,云南 昆明 650500昆明医科大学第一附属医院麻醉科,云南 昆明 650000昆明医科大学第一附属医院麻醉科,云南 昆明 650000
医药卫生
脑缺血再灌注损伤巨噬细胞小胶质细胞小胶质细胞极化代谢重编程
cerebral ischemia-reperfusion injurymacrophagesmicrogliamicroglia polarizationmetabolic reprogramming
《解放军医学杂志》 2026 (3)
435-442,8
This work was supported by the National Natural Science Foundation of China(82401716,82460252),and the Science and Technology Program of Department of Science and Technology of Yunnan Province(202201AY070001-037) 国家自然科学基金(82401716,82460252)云南省科技厅科技计划项目(202201AY070001-037)
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