Danggui Niantongtang in Treatment of Rheumatoid Arthritis： A Review
10.13422/j.cnki.syfjx.20252403
- VernacularTitle:当归拈痛汤治疗类风湿关节炎的研究进展
- Author:
Enhui ZHOU
1
;
Zhiying CHE
1
;
Zhenliang WANG
1
;
Erping XU
1
Author Information
1. Henan University of Chinese Medicine， Zhengzhou 450046， China
- Publication Type:Journal Article
- Keywords:
Danggui Niantongtang;
rheumatoid arthritis;
damp-heat stagnation syndrome;
clinical efficacy;
experimental research
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(11):343-349
- CountryChina
- Language:Chinese
-
Abstract:
Rheumatoid arthritis （RA） is a chronic systemic autoimmune disease characterized by symmetrical polyarthritis， which may lead to joint deformity and loss of joint function in the long term， severely impairing patients' quality of life. Danggui Niantongtang， originated from Medical Revelations by Zhang Yuansu in the Jin Dynasty， has the effects of clearing heat and draining dampness， dispelling wind and alleviating pain， and serves as a classic formula for treating RA damp-heat stagnation syndrome. By searching CNKI， Wanfang， PubMed and other databases， the author systematically reviewed the clinical efficacy and experimental research of Danggui Niantongtang in the treatment of RA， and elucidated its mechanisms of action， so as to provide a valuable reference for future clinical and basic research of Danggui Niantongtang in the field of RA. Clinical studies demonstrated that Danggui Niantongtang can improve core symptoms in RA patients with the damp-heat stagnation syndrome， including joint swelling and pain， morning stiffness and limited joint mobility， decrease inflammatory markers such as C-reactive protein （CRP） and erythrocyte sedimentation rate （ESR）， and facilitate postoperative rehabilitation in RA patients undergoing total knee arthroplasty （TKA）. When combined with Western medicines such as methotrexate， it can enhance the anti-inflammatory efficacy and mitigate adverse reactions， including gastrointestinal discomfort and hepatic injury. Experimental studies revealed that this formula can modulate the inflammatory cytokine network， promote synoviocyte apoptosis， inhibit abnormal synoviocyte autophagy， suppress synovial angiogenesis， and maintain intestinal flora homeostasis. However， several limitations exist in current research， such as insufficient clinical quality， unclear interaction between mechanisms and networks， and insufficient research on dosage form optimization. In the future， high-quality clinical research， multi-omics mechanistic studies， and dosage form improvement are needed to provide scientific basis for its clinical promotion and in-depth research.
