Tripterygium glycosides inhibit inflammatory mediators in the rat synovial RSC‑364 cell line stimulated with interleukin‑1β

Cai,Anji; Qi,Suwen; Su,Zhuowa; Shen,Huaqing; Ma,Wengsong; Dai,Yong

doi:10.3892/br.2015.501

Tripterygium glycosides inhibit inflammatory mediators in the rat synovial RSC‑364 cell line stimulated with interleukin‑1β

Authors:
- Anji Cai
- Suwen Qi
- Zhuowa Su
- Huaqing Shen
- Wengsong Ma
- Yong Dai
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Affiliations: Department of Clinical Laboratory, Nanshan Affiliated Hospital of Guangdong Medical College, Shenzhen, Guangdong 518020, P.R. China, Department of Biomedical Engineering, Medical School, Shenzhen University, Shenzhen, Guangdong 518020, P.R. China, The Second Clinical Medical College, Jinan University, Shenzhen People's Hospital, Shenzhen, Guangdong 518020, P.R. China
Published online on: August 4, 2015 https://doi.org/10.3892/br.2015.501
Pages: 763-766

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Abstract

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.

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