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Mediators of Inflammation
Volume 2014, Article ID 392062, 10 pages
Research Article

A Natural Flavonoid Glucoside, Icariin, Regulates Th17 and Alleviates Rheumatoid Arthritis in a Murine Model

1School of Pharmaceutical Science and Technology, Tianjin University, Office A508, Building 24, 92 Weijin Road, Nankai District, Tianjin 300072, China
2Haidian Maternal & Child Health Hospital of Beijing, China

Received 14 July 2014; Accepted 20 August 2014; Published 13 October 2014

Academic Editor: Julio Galvez

Copyright © 2014 Liqun Chi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that causes deformity of the joints and physical disability. Icariin, a natural flavonoid glucoside isolated from plants in the Epimedium family, has been proven to have various pharmacological activities. A recent study showed that icariin suppressed cartilage and bone degradation in mice of collagen-induced arthritis. However, the mechanism needs to be further investigated. In our current study, we found that icariin reduced the arthritis score and the incidence of arthritis compared with that in mice treated with water. Icariin inhibits the expression of various osteoclastogenic markers, such as β3 integrin, cathepsin K, and MMP9 in vitro. Icariin treatment in mice with CIA also resulted in less number of Th17 cells and decreased ratio of CD4+IL-17+ cells. The alleviated arthritis score and incidence of arthritis and reduced serum levels of IgG2a induced by icariin were abolished with additional IL-17 administration. Furthermore, icariin inhibited STAT3 activation in T cells and STAT3 inhibitor resulted in decreased IL-17 production and alleviated RA. In conclusion, icariin decreases Th17 cells and suppresses the production of IL-17, which contributes to the alleviated rheumatoid arthritis, through the inhibition of STAT3 activation.