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小胶质细胞介导的中风后中枢性疼痛的研究进展

Progress of research into microglial mediation of central post-stroke pain.

作者信息

Li Yue-Rong, Dang Zhao-Hui, Li Shan-Shan, Li Guang-Ya, Cai Hao-Bin, Lu Yun-Wei, Xie Lin-Lin, Li Li-Ling, Huang Liu-Ling, Qin Xiu-De, Bu Fan

机构信息

Department of Neurology & Psychology, Shenzhen Traditional Chinese Medicine Hospital, The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine, Shenzhen, Guangdong.

出版信息

Int J Immunopathol Pharmacol. 2024 Jan-Dec;38:3946320241309220. doi: 10.1177/03946320241309220.

DOI:10.1177/03946320241309220
PMID:39699048
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11660280/
Abstract

Central post-stroke pain (CPSP) is a chronic neuropathic pain syndrome that commonly occurs after cerebral stroke, and it severely impairs the daily activities of stroke patients. A number of fundamental and clinical studies support the theory that CPSP is mainly caused by ischemic and hemorrhagic injury of the spinal-thalamic-cortical neural pathway. However, the underlying reasons of CPSP genesis and development are far from clear. In recent years, the majority of research focused on microglia, the main resident immune cells of the central nervous system, which highlighted its critical role in the regulation of CPSP. The present article concentrated on exciting discoveries of microglia in mediating CPSP from the perspectives of their bioactive factors, cellular receptors, and signaling pathways, in order to offer a convenient and easy-to-digest overview. In addition, the potential and challenges of several agents in clinical translation of CPSP treatment was discussed based on recent preclinical studies.

摘要

中风后中枢性疼痛（CPSP）是一种常见于脑中风后的慢性神经性疼痛综合征，严重影响中风患者的日常活动。大量基础和临床研究支持CPSP主要由脊髓丘脑皮质神经通路的缺血性和出血性损伤引起这一理论。然而，CPSP发生和发展的根本原因仍远未明确。近年来，大多数研究聚焦于小胶质细胞，它是中枢神经系统主要的常驻免疫细胞，这突出了其在CPSP调节中的关键作用。本文从生物活性因子、细胞受体和信号通路等角度，集中探讨了小胶质细胞在介导CPSP方面的激动人心的发现，以便提供一个方便且易于理解的概述。此外，还基于近期的临床前研究讨论了几种药物在CPSP治疗临床转化中的潜力和挑战。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b72d/11660280/d5109ffb294f/10.1177_03946320241309220-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b72d/11660280/cf7305dd2284/10.1177_03946320241309220-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b72d/11660280/d5109ffb294f/10.1177_03946320241309220-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b72d/11660280/cf7305dd2284/10.1177_03946320241309220-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b72d/11660280/d5109ffb294f/10.1177_03946320241309220-fig2.jpg

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本文引用的文献

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CXCL12/CXCR4 Axis Promotes the Chemotaxis and Phagocytosis of B Cells through the PI3K-AKT Signaling Pathway in an Early Vertebrate.CXCL12/CXCR4 轴通过 PI3K-AKT 信号通路促进早期脊椎动物 B 细胞的趋化和吞噬作用。
J Immunol. 2024 Dec 1;213(11):1676-1690. doi: 10.4049/jimmunol.2300562.
2
The P2X7 Hypothesis of Central Post-Stroke Pain.中枢性卒中后疼痛的 P2X7 假说。
Int J Mol Sci. 2024 Jun 14;25(12):6577. doi: 10.3390/ijms25126577.
3
Blocking Pannexin-1 Channels Alleviates Thalamic Hemorrhage-Induced Pain and Inflammatory Depolarization of Microglia in Mice.
阻断 Pannexin-1 通道可减轻小鼠丘脑出血诱导的疼痛和小胶质细胞的炎症去极化。
ACS Chem Neurosci. 2023 Jul 19;14(14):2548-2559. doi: 10.1021/acschemneuro.3c00217. Epub 2023 Jun 28.
4
Research Progress on the Mechanisms of Central Post-Stroke Pain: A Review.中枢性脑卒中后疼痛的发病机制研究进展：综述。
Cell Mol Neurobiol. 2023 Oct;43(7):3083-3098. doi: 10.1007/s10571-023-01360-6. Epub 2023 May 11.
5
Combination of single-nucleus and bulk RNA-seq reveals the molecular mechanism of thalamus haemorrhage-induced central poststroke pain.单细胞和 bulk RNA-seq 的联合分析揭示了丘脑出血引起的脑卒中后中枢性疼痛的分子机制。
Front Immunol. 2023 Apr 20;14:1174008. doi: 10.3389/fimmu.2023.1174008. eCollection 2023.
6
Palmitoylethanolamide in the Treatment of Chronic Pain: A Systematic Review and Meta-Analysis of Double-Blind Randomized Controlled Trials.棕榈酸乙醇酰胺治疗慢性疼痛：一项双盲随机对照试验的系统评价和荟萃分析。
Nutrients. 2023 Mar 10;15(6):1350. doi: 10.3390/nu15061350.
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