脑出血后小胶质细胞极化及其相关炎症信号通路对继发性脑损伤的影响 Impact of Microglia Polarization and Related Inflammatory Signaling Pathways on Secondary Brain Injury after Intracerebral Hemorrhage

Autor: 孔德敏1,邹伟
Jazyk: čínština
Rok vydání: 2023
Předmět:
Zdroj: Zhongguo cuzhong zazhi, Vol 18, Iss 11, Pp 1315-1323 (2023)
Druh dokumentu: article
ISSN: 1673-5765
14217465
DOI: 10.3969/j.issn.1673-5765.2023.11.015
Popis: 脑出血是一种由脑实质血管破裂引起的严重疾病,目前尚无有效的治疗方法。研究表明炎症反应在脑出血继发性脑损伤中发挥了重要作用。在出血部位,小胶质细胞被迅速招募并激活,且在促炎型与抑炎型之间动态转变,不同的信号通路可以改变小胶质细胞极化的状态,从而对脑损伤起到调控作用,这提示了小胶质细胞在脑出血继发脑损伤的病理过程中具有复杂的作用机制。促炎型小胶质细胞释放的各种炎症因子介导神经细胞和神经组织的炎症损伤;抑炎型小胶质细胞释放趋化因子、脑源性神经营养因子、抗炎介质等诱导小胶质细胞向病变方向迁移,吞噬有害分子和细胞碎片,减轻炎症损伤,促进炎症消退、组织修复及神经再生。然而,目前对于小胶质细胞极化在脑出血后的动态变化及机制尚未完全阐明,故对参与脑出血小胶质细胞极化的相关调控分子以及信号通路的研究已引起了广泛关注,有望成为脑出血治疗的潜在靶点。 Abstract: Intracerebral hemorrhage is a severe condition caused by the rupture of blood vessels in the brain parenchyma, and currently lacks an effective treatment. Studies showed that inflammatory reactions play a crucial role in the brain damage that occurs as a result of intracerebral hemorrhage. Microglia, present at the site of bleeding, are rapidly recruited and activated, transitioning between pro-inflammatory and anti-inflammatory states. The polarization state of microglia can be altered by various signaling pathways, thus regulating the extent of brain damage. This suggests that microglia have a complex mechanism of action in the pathological process of secondary brain injury following intracerebral hemorrhage. Pro-inflammatory microglia release inflammatory factors that contribute to damage in nerve cells and nervous tissue, while anti-inflammatory microglia release chemokines, brain-derived neurotrophic factors, and anti-inflammatory mediators to induce the migration of microglia towards the lesion site. These microglia then phagocytose harmful molecules and cell debris, reducing inflammatory damage and promoting inflammation resolution, tissue repair, and nerve regeneration. However, the dynamic changes and mechanisms underlying microglial polarization after intracerebral hemorrhage have not been fully elucidated. Therefore, there is widespread interest in studying the regulatory molecules and signaling pathways involved in microglial polarization after intracerebral hemorrhage, as they may serve as potential targets for the treatment of intracerebral hemorrhage.
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