Therapeutic effect of neohesperidin on TNF-α-stimulated human rheumatoid arthritis fibroblast-like synoviocytes.
10.1016/S1875-5364(21)60107-3
- Author:
Xiao-He WANG
1
,
2
;
Ce DAI
3
;
Jun WANG
3
;
Rui LIU
3
;
Lei LI
3
;
Zong-Sheng YIN
4
Author Information
1. Department of Bone and Joint Surgery, Institute of Orthopedic Diseases, the First Affiliated Hospital, Jinan University, Guangzhou 510000, China
2. Department of Orthopedics, the First Affiliated Hospital of Anhui Medical University, Hefei 230000, China.
3. Department of Orthopedics, the First Affiliated Hospital of Anhui Medical University, Hefei 230000, China.
4. Department of Orthopedics, the First Affiliated Hospital of Anhui Medical University, Hefei 230000, China. Electronic address: anhuiyzs@126.com.
- Publication Type:Journal Article
- Keywords:
Fibroblast-like synoviocytes;
Inflammatory;
MAPK;
Neohesperidin;
Oxidative stress;
Rheumatoid-arthritis
- MeSH:
Arthritis, Rheumatoid/drug therapy*;
Cell Movement;
Cell Proliferation;
Cells, Cultured;
Fibroblasts;
Hesperidin/analogs & derivatives*;
Humans;
Synoviocytes;
Tumor Necrosis Factor-alpha/genetics*
- From:
Chinese Journal of Natural Medicines (English Ed.)
2021;19(10):741-749
- CountryChina
- Language:English
-
Abstract:
During the pathogensis of rheumatoid arthritis (RA), activated RA fibroblast-like synoviocytes (RA-FLSs) combines similar proliferative features as tumor and inflammatory features as osteoarthritis, which eventually leads to joint erosion. Therefore, it is imperative to research and develop new compounds, which can effectively inhibit abnormal activation of RA-FLSs and retard RA progression. Neohesperidin (Neo) is a major active component of flavonoid compounds with anti-inflammation and anti-oxidant properties. In this study, the anti-inflammation, anti-migration, anti-invasion, anti-oxidant and apoptosis-induced effects of Neo on RA-FLSs were explored to investigate the underlying mechanism. The results suggested that Neo decreased the levels of interleukin IL-1β, IL-6, IL-8, TNF-α, MMP-3, MMP-9 and MMP-13 in FLSs. Moreover, Neo blocked the activation of the MAPK signaling pathway. Furthermore, treatment with Neo induced the apoptosis of FLSs, and inhibited the migration of FLSs. It was also found that Neo reduced the accumulation of reactive oxygen species (ROS) induced by TNF-α. Taken together, our results highlighted that Neo may act as a potential and promising therapeutic drug for the management of RA.
