Wang-Bi tablet, a patented Chinese medicine, maintains the balance of Th1/Th2 in mice with collagen-induced arthritis

被引:0
|
作者
Wang Jianming [1 ]
Luo Jing [1 ]
Xu Yuan [1 ]
Yan Zeran [1 ]
Qu Xiangke [2 ]
Chen Mengxue [2 ]
Tao Qingwen [1 ]
机构
[1] China Japan Friendship Hosp, Dept Rheumatol Tradit Chinese Med, Beijing 100029, Peoples R China
[2] Beijing Univ Chinese Med, Integrat Chinese & Western Med Excellence, Beijing 100029, Peoples R China
关键词
Arthritis; rheumatoid; Collagen; Th1-Th2; balance; Wang-Bi tablet; RHEUMATOID-ARTHRITIS; TRANSCRIPTION FACTOR; T-BET; TH1; CELLS;
D O I
暂无
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
OBJECTIVE: To investigate the pharmacological mechanism of Wang-Bi tablets (WBTs), a Chinese patented medicine, in rheumatoid arthritis (RA) using mice with collagen-induced arthritis (CIA). METHODS: A mouse model of CIA was induced using bovine type IT collagen. WBT treatment was administered and efficacy was evaluated. The levels of interferon-gamma (IFN-gamma), interleukin-2 (IL-2), and interleukin-4 (IL-4) were examined using an enzyme-linked immunosorbent assay, and the proportions of Th1 and Th2 were detected using flow cytometry. T-bet and GATA-binding protein 3 (GATA3) expression were demonstrated using Western blot analysis. RESULTS: Paw swelling and the arthritis index decreased significantly following WBT treatment. Histopathological analysis revealed markedly alleviated damage to synovium tissue in the WBT and methotrexate treatment groups. WBT regulated the production of IFN-gamma, IL-2, and IL-4 and modulated Th1 and Th2 cell populations, which might have been induced by the attenuation of Th1 and Th2 cell differentiation through a decrease in the expression of T-bet and an increase in the expression of GATA3 in the synovial tissue in CIA mice. CONCLUSION: These results indicate that WBT may produce a therapeutic effect on CIA through maintaining the balance of Th1/Th2 cells, which could result in a decrease in the autoinflammatory disorder observed in RA. (C) 2020 JTCM. All rights reserved.
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收藏
页码:401 / 406
页数:6
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