Chlorogenic Acid Inhibits BAFF Expression in Collagen-Induced Arthritis and Human Synoviocyte MH7A Cells by Modulating the Activation of the NF-κB Signaling Pathway. (22nd May 2019)

• Record Type: Journal Article
• Authors: Fu, Xiaohong; Lyu, Xilin; Liu, Han; Zhong, Dan; Xu, Zhizhen; He, Fengtian; Huang, Gang
• Other Names: Kolarz Bogdan Academic Editor.
• Is Part Of: Journal of immunology research. Volume 2019(2019)
• Publication Date: 2019-05-22
• Subjects: Immunology -- Periodicals; Immunology -- Research -- Periodicals; 616.07905
• DOI: 10.1155/2019/8042097
• Languages: English
• ISSNs: 2314-8861

Abstract

Abstract : B cell activating factor (BAFF), a member of the tumor necrosis factor (TNF) family, plays a critical role in the pathogenesis and progression of rheumatoid arthritis (RA). Chlorogenic acid (CGA) is a phenolic compound and exerts antiarthritic activities in arthritis. However, it is not clear whether the anti-inflammatory property of CGA is associated with the regulation of BAFF expression. In this study, we found that treatment of the collagen-induced arthritis (CIA) mice with CGA significantly attenuated arthritis progression and markedly inhibited BAFF production in serum as well as the production of serum TNF- α . Furthermore, CGA inhibits TNF- α -induced BAFF expression in a dose-dependent manner and apoptosis in MH7A cells. Mechanistically, we found the DNA-binding site for the transcription factor NF- κ B in the BAFF promoter region is required for this regulation. Moreover, CGA reduces the DNA-binding activity of NF- κ B to the BAFF promoter region and suppresses BAFF expression through the NF- κ B pathway in TNF- α -stimulated MH7A cells. These results suggest that CGA may serve as a novel therapeutic agent for the treatment of RA by targeting BAFF.