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Updated: Nov 28, 2025

Generation of Induced-pluripotent Stem Cells Using Fibroblast-like Synoviocytes Isolated from Joints of Rheumatoid Arthritis Patients
Published on: October 16, 2016
Diosgenin Inhibits Excessive Proliferation and Inflammatory Response of Synovial Fibroblasts in Rheumatoid Arthritis
Roujun Wang1, Yumeng Sun2, Xiaowen Jin2
1Department of Diabetes and Endocrinology, Kunming Municipal Hospital of Traditional Chinese Medicine, Kunming, 650500, Yunnan, China.
Diosgenin effectively reduces rheumatoid arthritis (RA) synovial cell proliferation and inflammation. This natural compound targets PDE3B, offering a potential therapeutic mechanism for RA joint abnormalities.
Area of Science:
- Biochemistry
- Immunology
- Pharmacology
Background:
- Rheumatoid arthritis (RA) is a chronic inflammatory condition causing joint damage.
- Synovial cell abnormalities, including excessive proliferation and inflammation, are key features of RA.
- Diosgenin is recognized for its anti-inflammatory properties.
Purpose of the Study:
- To investigate the effects and mechanisms of diosgenin on RA synovial cell proliferation and inflammation.
- To elucidate the role of phosphodiesterase 3B (PDE3B) in diosgenin's therapeutic action.
Main Methods:
- Cell viability assessed using CCK-8 assays.
- Apoptosis and protein expression analyzed via TUNEL assays and Western blotting.
- Cell migration and inflammatory cytokine levels measured using wound healing assays and ELISA kits.
Main Results:
- Diosgenin significantly inhibited proliferation and migration of RA synovial cells.
- Diosgenin reduced inflammatory responses in RA synovial cells.
- Downregulation of PDE3B expression was observed with diosgenin treatment, and its overexpression reversed diosgenin's effects.
Conclusions:
- Diosgenin demonstrates therapeutic potential by inhibiting excessive proliferation and inflammatory responses of RA synovial fibroblasts.
- Targeting PDE3B is a key mechanism through which diosgenin exerts its anti-RA effects.
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