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中华针灸电子杂志 ›› 2024, Vol. 13 ›› Issue (02) : 73 -77. doi: 10.3877/cma.j.issn.2095-3240.2024.02.007

综述

小胶质细胞在缺血性卒中后脑白质损伤中的作用及针刺干预机制
高琪1, 彭拥军1,()   
  1. 1. 210029 南京中医药大学附属医院针灸康复科
  • 收稿日期:2023-10-28 出版日期:2024-05-15
  • 通信作者: 彭拥军
  • 基金资助:
    国家自然科学基金项目(82174484,81973932); 江苏省中医院高峰学术人才项目(k2021rc24); 江苏省第六期"333高层次人才培养工程"

The role of microglia in white matter injury after ischaemic stroke and the mechanism of acupuncture intervention

Qi Gao1, Yongjun Peng1,()   

  1. 1. Department of Acupuncture and Rehabilitation, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China
  • Received:2023-10-28 Published:2024-05-15
  • Corresponding author: Yongjun Peng
引用本文:

高琪, 彭拥军. 小胶质细胞在缺血性卒中后脑白质损伤中的作用及针刺干预机制[J/OL]. 中华针灸电子杂志, 2024, 13(02): 73-77.

Qi Gao, Yongjun Peng. The role of microglia in white matter injury after ischaemic stroke and the mechanism of acupuncture intervention[J/OL]. Chinese Journal of Acupuncture and Moxibustion(Electronic Edition), 2024, 13(02): 73-77.

缺血性卒中后脑白质损伤是导致卒中后长期感觉运动障碍和认知障碍的重要原因,脑白质在卒中后神经恢复中的关键作用不容忽视。目前研究表明小胶质细胞可调控中枢免疫炎症反应,在缺血性卒中诱导的脑白质损伤中起着加重损伤和促进修复的双重作用,而针刺通过调节小胶质细胞达到改善缺血性卒中后脑白质损伤结局的可能干预机制近来颇受关注。其干预机制主要通过抑制Toll样受体4信号通路、抑制基质金属蛋白酶-9的表达、促进膜联蛋白1和髓细胞触发受体2的表达等途径发挥改善炎症环境、促进髓鞘修复与再生的作用。

Cerebral white matter injury is a significant contributor to enduring sensorimotor and cognitive impairments post stroke. Microglia are pivotal in modulating immune-inflammatory responses within the central nervous system and play a dual role in both exacerbating injury and facilitating repair in cases of ischaemic stroke-induced white matter injury. This highlights the potential efficacy of acupuncture as a therapeutic intervention target these mechanisms. Recently, the potential mechanism of acupuncture in improving the prognosis of white matter injury post ischemic stroke through the regulation of microglia has attracted much attention. Acupuncture mainly ameliorates the inflammatory milieu and facilitates myelin regeneration and repair by suppressing the TLR4 signaling pathway, reducing MMP-9 expression, and promoting the expression of ANXA1 and TERM2.

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