中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (2): 443-454.doi: 10.4103/NRR.NRR-D-24-01166

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

小胶质细胞在缺血性脑卒中中的作用及干预策略

  

  • 出版日期:2026-02-15 发布日期:2025-05-17
  • 基金资助:
    国家自然科学基金项目，编号： 82471345；江苏省科技厅社会发展重点研发计划项目，江苏省科学技术厅社会发展重点研究发展计划，编号：BE2022668

Microglial intervention in ischemic stroke: Roles and intervention strategies

Cuiling Ji# , Lixinbei Sheng# , Kaijun Han# , Ping Yuan, Wei Li, Lu Chen* , Yongyue Gao*   

  1. Department of Neurosurgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu Province, China
  • Online:2026-02-15 Published:2025-05-17
  • Contact: Lu Chen, PhD, gycc2011@126.com; Yongyue Gao, PhD, tallergao@163.com.
  • Supported by:
    This review was supported by the National Natural Science Foundation of China, 82471345 (to LC); the Key Research and Development Program for Social Development by the Jiangsu Provincial Department of Science and Technology. No. BE2022668 (to LC).

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摘要：

缺血性脑卒中是导致神经功能缺损和高度残疾的主要原因。作为中枢神经系统的核心免疫细胞，小胶质细胞具有神经炎症和卒中后组织修复的双重功能，其动态激活和极化状态是影响疾病进程和治疗结果的关键因素。文章探讨了小胶质细胞在缺血性脑卒中中的作用及潜在的干预策略。小胶质细胞表现出一种动态功能状态，在促炎(M1)和抗炎(M2)表型之间转换。这种双重性通过维持神经炎症和组织修复之间的平衡在脑梗死中发挥着关键作用。活化的小胶质细胞通过释放细胞因子和破坏血脑屏障导致神经炎症，同时也通过抗炎反应和再生促进组织修复。影响小胶质细胞活化的关键途径包括 TLR4/核转录因子κB、MAPK、JAK/STAT 和 PI3K/AKT/mTOR。这些通路是各种旨在促进 M2 极化和减少损伤的实验疗法的靶点，包括米诺环素等药物中的天然化合物以及传统中药。针对这些调控机制的药物，如小分子抑制剂和中药成分，以及新兴的单细胞RNA测序和空间转录组学技术，为缺血性脑卒中提供了新的治疗思路和临床转化潜力。

https://orcid.org/0000-0002-0170-8778 (Lu Chen); https://orcid.org/0009-0005-3577-6444 (Yongyue Gao)

关键词: 血脑屏障, 缺血性脑卒中, 小胶质细胞, 神经再生, 神经炎症, 神经保护, 氧化应激, 极化, 信号通路, 治疗策略

Abstract: Ischemic stroke is a major cause of neurological deficits and high disability rate. As the primary immune cells of the central nervous system, microglia play dual roles in neuroinflammation and tissue repair following a stroke. Their dynamic activation and polarization states are key factors that influence the disease process and treatment outcomes. This review article investigates the role of microglia in ischemic stroke and explores potential intervention strategies. Microglia exhibit a dynamic functional state, transitioning between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes. This duality is crucial in ischemic stroke, as it maintains a balance between neuroinflammation and tissue repair. Activated microglia contribute to neuroinflammation through cytokine release and disruption of the blood–brain barrier, while simultaneously promoting tissue repair through anti-inflammatory responses and regeneration. Key pathways influencing microglial activation include Toll-like receptor 4/nuclear factor kappa B, mitogen-activated protein kinases, Janus kinase/signal transducer and activator of transcription, and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways. These pathways are targets for various experimental therapies aimed at promoting M2 polarization and mitigating damage. Potential therapeutic agents include natural compounds found in drugs such as minocycline, as well as traditional Chinese medicines. Drugs that target these regulatory mechanisms, such as small molecule inhibitors and components of traditional Chinese medicines, along with emerging technologies such as single-cell RNA sequencing and spatial transcriptomics, offer new therapeutic strategies and clinical translational potential for ischemic stroke.

Key words: blood–brain barrier,  ischemic stroke,  microglia,  nerve regeneration,  neuroinflammation,  neuroprotection,  oxidative stress,  polarization,   signaling pathways,  therapeutic strategies