Open AccessTripterygium glycosides inhibit inflammatory mediators in the rat synovial RSC-364 cell line stimulated with interleukin-1β
Author(s) -
Aizhen Cai,
Suwen Qi,
Ziyi Su,
Huaqing Shen,
Wengsong Ma,
Yong Dai
Publication year - 2015
Publication title -
biomedical reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.607
H-Index - 25
eISSN - 2049-9442
pISSN - 2049-9434
DOI - 10.3892/br.2015.501
Subject(s) - tripterygium , inflammation , matrix metalloproteinase , chromatin structure remodeling (rsc) complex , interleukin , cell cycle , apoptosis , medicine , proinflammatory cytokine , cell , pharmacology , oncogene , chemistry , cytokine , immunology , glycoside , biochemistry , gene expression , stereochemistry , chromatin remodeling , gene
Tripterygium glycosides (TG) are extracted from a traditional Chinese medicinal herb. Using the compound, progress has been made in the treatment of rheumatoid arthritis (RA), but the underlying mechanism of its action is poorly understood. The purpose of the present study was to investigate the role of TG in preventing inflammatory arthritis. An inflammatory cell model was established in the rat synovial RSC-364 cell line via induction with interleukin (IL)-1β. The expression of IL-32 and matrix metalloproteinases (MMP-1 and MMP-9) was determined using an enzyme-linked immunosorbent assay. Compared with the control group (without IL-1β), IL-1β in the treatment group induced the expression of IL-32, MMP-1 and MMP-9 in RSC-364 cells. When a different dose of TG was added to RSC-364 cells stimulated with IL-1β, TG decreased the expression levels of IL-32, MMP-1 and MMP-9 in a dose-dependent manner. These results indicated that TG suppressed the inflammation response in RSC-364 cells. Taken together, these findings may contribute to a better understanding of the role of TG in the anti-inflammatory therapeutics for RA.