1.内蒙古医科大学中医临床医学院,呼和浩特 010107
2.鄂尔多斯市中医医院风湿病科,内蒙古 鄂尔多斯 017010
3.内蒙古自治区中医医院风湿病科,呼和浩特 010020
Received:22 October 2025,
Revised:2026-02-23,
Accepted:25 February 2026,
Published:30 March 2026
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王祚,刘禹欣,乔雨欣,等.中药调控炎症微环境干预骨关节炎的机制研究进展 [J].中国药房,2026,37(06):823-828.
WANG Zuo,LIU Yuxin,QIAO Yuxin,et al.Research progress on the mechanism of traditional Chinese medicine intervening in osteoarthritis by modulating the inflammatory microenvironment[J].ZHONGGUO YAOFANG,2026,37(06):823-828.
王祚,刘禹欣,乔雨欣,等.中药调控炎症微环境干预骨关节炎的机制研究进展 [J].中国药房,2026,37(06):823-828. DOI: 10.6039/j.issn.1001-0408.2026.06.22.
WANG Zuo,LIU Yuxin,QIAO Yuxin,et al.Research progress on the mechanism of traditional Chinese medicine intervening in osteoarthritis by modulating the inflammatory microenvironment[J].ZHONGGUO YAOFANG,2026,37(06):823-828. DOI: 10.6039/j.issn.1001-0408.2026.06.22.
炎症微环境与骨关节炎的发生发展密切相关,其具体可表现为巨噬细胞激活、炎症因子紊乱及氧化还原失衡。本文在概述骨关节炎炎症微环境病理特征的基础上,综述了中药调控炎症微环境干预骨关节炎的机制研究进展,发现中药单体/有效部位(马钱子总生物碱、槲皮素、雷公藤甲素等)、药对(独活-秦艽药对、红花-伸筋草药对)以及复方(壮骨健膝方、独活寄生汤、荣筋拈痛方等)可通过抑制核因子κB、Wnt/
β
-联蛋白、丝裂原活化蛋白激酶等多条信号通路,抑制巨噬细胞异常活化、减少促炎性细胞因子释放和活性氧生成等多维度来系统干预炎症微环境,重塑关节局部稳态,从而延缓骨关节炎进展。
The inflammatory microenvironment is closely associated with the initiation and progression of osteoarthritis (OA), specifically manifesting as macrophage activation, dysregulation of inflammatory cytokines, and redox imbalance. Following an overview of the pathological characteristics of the OA inflammatory microenvironment, this paper reviews the research progress on the mechanism of traditional Chinese medicine (TCM) intervening in OA by modulating the inflammatory microenvironment. It has been found that TCM monomers/active ingredients (such as total alkaloids from
Strychnos nux-vomica
, quercetin, triptolide, etc.), herb pairs (e.g.
Angelica pubescens
-
Gentiana macrophylla
, Carthami Flos-Lycopodii Herba), and TCM formulas (such as Zhuanggu jianxi formula, Duhuo jisheng decoction and Rongjin niantong formula, etc.) can inhibit macrophage activation, reduce the release of proinflammatory cytokines and the generation of reactive oxygen species by inhibiting multiple signaling pathways, including nuclear factor-κB, Wnt/
β
-catenin, and mitogen-activated protein kinase, thereby alleviating the articular inflammatory microenvironment, restoring local joint homeostasis, and slowing the progression of OA.
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