当期文章

NLRP3炎症小体调控慢性疼痛机制的研究进展

杨宗芝^1,2, 武婕¹, 黄小兰¹, 熊东林³, 罗裕辉³, 肖礼祖³, 樊碧发⁴, 蒋昌宇^1,3,*

¹广东医科大学第一临床医学院，湛江 524023；²河源市妇幼保健院麻醉科，河源 517000；³深圳市南山区人民医院疼痛科，深圳 518052；⁴中日友好医院疼痛科，北京 100029

摘要

NLRP3炎症小体作为先天免疫系统的核心效应器，在慢性疼痛的发生与维持过程中发挥关键调控作用。研究表明，在多种慢性疼痛模型中，NLRP3 炎症小体在外周神经系统，尤其是背根神经节(dorsal root ganglion, DRG)中被激活，促进白介素1β (interleukin-1β, IL-1β)等促炎介质的释放，增强感觉神经元的兴奋性，从而加剧伤害性信号的传导与放大。同时，DRG内的卫星胶质细胞及浸润的免疫细胞共同参与炎症微环境的形成，构建起“神经-胶质-免疫”协同促痛网络。在中枢神经系统中，NLRP3 炎症小体主要通过激活脊髓小胶质细胞和星形胶质细胞诱导突触可塑性改变和中枢敏化，进一步推动疼痛信号的异常增强。本文综述了近年来关于NLRP3 炎症小体在外周及中枢神经系统中调控慢性疼痛机制的研究进展，为探索靶向炎症小体的镇痛新策略提供理论依据。

关键词： NLRP3炎症小体; 慢性疼痛; 机制; 神经炎症; 神经胶质细胞

Mechanistic insights into NLRP3 inflammasome regulation of chronic pain

YANG Zong-Zhi^1,2, WU Jie¹, HUANG Xiao-Lan¹, XIONG Dong-Lin³, LUO Yu-Hui³, XIAO Li-Zu³, FAN Bi-Fa⁴, JIANG Chang-Yu^1,3,*

¹First School of Clinical Medicine, Guangdong Medical University, Zhanjiang 524023, China；²Department of Anesthesiology, Heyuan Maternal and Child Health Hospital, Heyuan 517000, China；³Pain Department, Shenzhen Nanshan People's Hospital, Shenzhen 518052, China；⁴Pain Department, China-Japan Friendship Hospital, Beijing 100029, China

Abstract

The NLRP3 inflammasome, a pivotal effector of the innate immune system, has emerged as a critical regulator in the initiation and maintenance of chronic pain. Accumulating evidence demonstrates that NLRP3 inflammasome activation in the peripheral nervous system, particularly in dorsal root ganglia (DRG), promotes the release of pro-inflammatory mediators such as interleukin-1β (IL-1β), enhances sensory neuronal excitability, and facilitates nociceptive signal transmission and amplification. Moreover, satellite glial cells and infiltrating immune cells within the DRG contribute to the establishment of an inflammatory microenvironment, forming a neuron-glia-immune network that drives pain sensitization. In the central nervous system, activation of the NLRP3 inflammasome in microglia and astrocytes induces alterations in synaptic plasticity and central sensitization, further exacerbating the aberrant amplification of pain signals. This review summarizes recent advances in elucidating the regulatory mechanisms of the NLRP3 inflammasome in chronic pain in both peripheral and central nervous systems, providing a theoretical foundation for the development of novel analgesic strategies targeting the inflammasome.

Key words: NLRP3 inflammasome; chronic pain; mechanism; neuroinflammation; glial cells

收稿日期：　　录用日期：

通讯作者：蒋昌宇　　E-mail:

DOI: 10.13294/j.aps.2026.0009

引用本文：

杨宗芝, 武婕, 黄小兰, 熊东林, 罗裕辉, 肖礼祖, 樊碧发, 蒋昌宇. NLRP3炎症小体调控慢性疼痛机制的研究进展[J]. 生理学报 2026; 78 (1): 135-147.

YANG Zong-Zhi, WU Jie, HUANG Xiao-Lan, XIONG Dong-Lin, LUO Yu-Hui, XIAO Li-Zu, FAN Bi-Fa, JIANG Chang-Yu. Mechanistic insights into NLRP3 inflammasome regulation of chronic pain. Acta Physiol Sin 2026; 78 (1): 135-147 (in Chinese with English abstract).