Gong Yuhua, Li Hui, Cui Huanglin, Gong Yuping
School of Smart Health, Chongqing Polytechnic University of Electronic Technology, Chongqing, 401331, People's Republic of China.
Ultrasound Department of the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, People's Republic of China.
J Inflamm Res. 2025 Feb 26;18:2955-2973. doi: 10.2147/JIR.S498809. eCollection 2025.
Intracerebral hemorrhage (ICH) is a particularly common public health problem with a high mortality and disability rate and no effective treatments to enhance clinical prognosis. The increased aging population, improved vascular prevention, and augmented use of antithrombotic agents have collectively contributed to the rise in ICH incidence over the past few decades. The exploration and understanding of mechanisms and intervention strategies has great practical significance for expanding treatments and improving prognosis of ICH. Microglia, as resident macrophages of central nervous system, are responsible for the first immune defense post-ICH. After ICH, M1 microglia is firstly activated by primary injury and thrombin; subsequently, reactive microglia can further amplify the immune response and exert secondary injury (eg, oxidative stress, neuronal damage, and brain edema). The pro-inflammatory phenotype transmits to M2 microglia within 7 days post-ICH, which plays a key role in erythrophagocytosis and limiting the inflammatory secondary injury. Microglial M2 polarization has significant implications for improving prognosis, this process can be mediated through crosstalk with other cells, metabolic changes, and microbiota interaction. Clarifying the effect, timing, and potential downstream effects of multiple mechanisms that synergistically trigger anti-inflammatory responses may be necessary for clinical translation. Analyses of such intricate interaction between microglia cells and brain injury/repair mechanisms will contribute to our understanding of the critical microglial responses to microenvironment and facilitating the discovery of appropriate intervention strategies. Here, we present a comprehensive overview of the latest evidences on microglial dynamics following ICH, their role in driving primary/secondary injury mechanisms as well as neurorepair/plasticity, and possible treatment strategies targeting microglia.
脑出血（ICH）是一个极为常见的公共卫生问题，死亡率和致残率很高，且尚无有效的治疗方法来改善临床预后。在过去几十年中，人口老龄化加剧、血管预防措施的改进以及抗血栓药物使用的增加，共同导致了脑出血发病率的上升。对脑出血发病机制和干预策略的探索与理解，对于拓展治疗方法和改善脑出血预后具有重大的现实意义。小胶质细胞作为中枢神经系统的常驻巨噬细胞，在脑出血后负责第一道免疫防御。脑出血后，M1小胶质细胞首先被原发性损伤和凝血酶激活；随后，反应性小胶质细胞可进一步放大免疫反应并造成继发性损伤（如氧化应激、神经元损伤和脑水肿）。促炎表型在脑出血后7天内转变为M2小胶质细胞，后者在吞噬红细胞和限制炎症继发性损伤中起关键作用。小胶质细胞M2极化对改善预后具有重要意义，这一过程可通过与其他细胞的相互作用、代谢变化和微生物群相互作用来介导。阐明协同触发抗炎反应的多种机制的作用、时机及潜在的下游效应，可能是实现临床转化所必需的。分析小胶质细胞与脑损伤/修复机制之间这种复杂的相互作用，将有助于我们理解小胶质细胞对微环境的关键反应，并促进合适干预策略的发现。在此，我们全面概述了脑出血后小胶质细胞动态变化的最新证据、它们在驱动原发性/继发性损伤机制以及神经修复/可塑性方面的作用，以及针对小胶质细胞的可能治疗策略。
