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Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 268065, 8 pages
http://dx.doi.org/10.1155/2013/268065
Research Article

Baicalin Inhibits IL-17-Mediated Joint Inflammation in Murine Adjuvant-Induced Arthritis

Xue Yang,1,2 Ji Yang,3 and Hejian Zou1,2

1Division of Rheumatology, Huashan Hospital, Fudan University, 12 Wulumuqizhong Road, Shanghai 200040, China
2Institute of Rheumatology, Immunology and Allergy, Shanghai Medical College, Fudan University, Huashan Hospital, Shanghai 200040, China
3Department of Dermatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China

Received 14 March 2013; Revised 22 May 2013; Accepted 22 May 2013

Academic Editor: Hiroshi Nakajima

Copyright © 2013 Xue Yang 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.

Abstract

T-helper-17 (Th17) cells are implicated in a number of inflammatory disorders including rheumatoid arthritis. Antagonism of Th17 cells is a treatment option for arthritis. Here, we report that Baicalin, a compound isolated from the Chinese herb Huangqin (Scutellaria baicalensis Georgi), relieved ankle swelling and protected the joint against inflammatory destruction in a murine adjuvant-induced arthritis model. Baicalin inhibited splenic Th17 cell population expansion in vivo. Baicalin prevented interleukin- (IL-) 17-mediated lymphocyte adhesion to cultured synoviocytes. Baicalin also blocked IL-17-induced intercellular adhesion molecule 1, vascular cell adhesion molecule 1, IL-6, and tumor necrosis factor-alpha mRNA expression in cultured synoviocytes. Collectively, these findings suggest that Baicalin downregulates the joint inflammation caused by IL-17, which is likely produced by an expanded population of splenic Th17 cells in experimental arthritis. Baicalin might be a promising novel therapeutic agent for treating rheumatoid arthritis in humans.