华中科技大学学报(医学版) ›› 2026, Vol. 55 ›› Issue (4): 579-585.doi: 10.3870/j.issn.1672-0741.26.01.012

• 综述 • 上一篇    下一篇

瞬时受体电位通道介导关节炎疼痛的神经机制与脉冲射频靶向调控的研究进展*

李鑫1, 王猛1, 陈晓东1, 华豪1, 徐同生1, 王存金2△   

  1. 1苏州大学附属无锡市第九人民医院麻醉科,无锡 214000
    2扬州大学医学部附属苏北人民医院麻醉科,扬州 225001
  • 收稿日期:2026-01-12 出版日期:2026-08-15 发布日期:2026-07-28
  • 通讯作者: E-mail:cunjinwang@163.com
  • 作者简介:李 鑫,男,1981生,副主任医师,E-mail:lixin13771189909@163.com
  • 基金资助:
    *国家自然科学基金资助项目(No.82171207);江苏省基础研究计划自然科学基金面上项目(No.BK20231246)

Research Progress on the Neuronal Mechanism of Arthritis Pain Mediated by Transient Receptor Potential Channels and Targeted Regulation by Pulsed Radiofrequency

Li Xin, Wang Meng, Chen Xiaodong, et al   

  1. Department of Anesthesiology,Wuxi Ninth People's Hospital Affiliated to Soochow University,Wuxi 214000,China
  • Received:2026-01-12 Online:2026-08-15 Published:2026-07-28
  • Contact: E-mail:cunjinwang@163.com

摘要: 慢性关节炎疼痛的治疗长期面临传统镇痛药物疗效不足与不良反应显著的临床挑战。脉冲射频(PRF)作为一种非破坏性神经调控技术,通过靶向瞬时受体电位(TRP)通道家族(如TRPV1、TRPA1和TRPM3)展现出独特潜力。该综述系统探讨PRF与TRP通道在关节炎疼痛中的交互机制:TRP作为疼痛感知的关键枢纽,在关节炎微环境(酸化、氧化应激及炎症因子)中持续激活,推动外周敏化向中枢敏化演进;PRF则借助非热生物学效应调控TRP功能,包括调节神经元膜电位与钙振荡,改善线粒体功能,与神经胶质交互,调节内源性阿片肽/γ-氨基丁酸(γ-aminobutyric acid,GABA)系统以抑制TRP通道家族活性。文章构建“PRF-TRP-关节炎疼痛”调控轴,提出TRP表达谱可作为PRF疗效的预测标志物,并阐释不同关节炎亚型对PRF响应差异的TRP依赖性机制。PRF已从单纯镇痛工具发展为神经可塑性调节器,其通过TRP通道整合神经-免疫-离子通道功能,推动关节炎治疗从抗炎模式转向神经稳态重建,为慢性疼痛管理提供了新路径。

关键词: 脉冲射频, 瞬时受体电位, 关节炎疼痛, 神经调控

Abstract: The treatment of chronic arthritic pain has long been confronted with clinical challenges,such as insufficient efficacy of traditional analgesic drugs and significant adverse reactions.As a non-destructive neuromodulation technique,pulsed radiofrequency(PRF)shows unique potential by targeting the transient receptor potential(TRP)channel family(TRPV1,TRPA1,and TRPM3).This review systematically explores the interaction mechanism between PRF and TRP channels in arthritic pain:As a key hub for pain perception,TRP channels are continuously activated in the arthritic microenvironment(characterized by acidification,oxidative stress,and inflammatory factors),which promotes the progression from peripheral sensitization to central sensitization.PRF regulates the function of TRP via non-thermal biological effects,including modulating neuronal membrane potential and calcium oscillation,improving mitochondrial function and neuroglial interaction,as well as regulating endogenous opioid peptide and γ-aminobutyric acid(GABA)systems to inhibit the activity of the TRP channel family.This study establishes the regulatory axis of "PRF-TRP-arthritic pain",proposes that TRP expression profiles can serve as predictive biomarkers for PRF efficacy,and elucidates the TRP-dependent mechanisms underlying differential responses to PRF among various arthritis subtypes.This article constructs a "PRF-TRP-arthritic pain" regulatory axis,proposes that the TRP expression profile may serve as a predictive marker for PRF efficacy,and elaborates on the TRP-dependent mechanism underlying the differential PRF responses among different arthritis subtypes.PRF has evolved from a simple analgesic tool to a regulator of neural plasticity.By integrating neuro-immune-ion channel functions through TRP channels,PRF promotes the transformation of arthritis treatment from an anti-inflammatory model to neural homeostasis reconstruction,thereby providing a new approach for chronic pain management.

Key words: pulsed radiofrequency, transient receptor potential, arthritic pain, neuromodulation

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