1. Diosgenin Inhibits Excessive Proliferation and Inflammatory Response of Synovial Fibroblasts in Rheumatoid Arthritis by Targeting PDE3B.
- Author
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Wang R, Sun Y, Jin X, Wen W, and Cao Y
- Subjects
- Apoptosis drug effects, Apoptosis Regulatory Proteins metabolism, Arthritis, Rheumatoid enzymology, Arthritis, Rheumatoid genetics, Arthritis, Rheumatoid pathology, Cell Movement, Cells, Cultured, Fibroblasts enzymology, Fibroblasts pathology, Humans, Signal Transduction, Synoviocytes enzymology, Synoviocytes pathology, Anti-Inflammatory Agents pharmacology, Arthritis, Rheumatoid drug therapy, Cell Proliferation drug effects, Cyclic Nucleotide Phosphodiesterases, Type 3 metabolism, Cytokines metabolism, Diosgenin pharmacology, Fibroblasts drug effects, Synoviocytes drug effects
- Abstract
Rheumatoid arthritis (RA) is a chronic inflammation that can lead to loss of range of joint abnormalities in severe cases. Diosgenin has anti-inflammatory effects. This paper discussed the effect and mechanism of diosgenin on excessive proliferation and inflammatory response of synovial cells in RA. CCK-8 detected the cell viability, TUNEL assay detected the apoptosis of cells and western blot detected the expression of apoptosis-related proteins. Wound healing was used to detect cell migration and western blot detected the expression of migration-related proteins. ELISA kits were used to detect the levels of inflammatory cytokines in cells. Diosgenin can inhibit the proliferation and migration of RA synovial cells. At the same time, diosgenin could reduce the inflammatory response of RA synovial cells, during which the expression of PDE3B was significantly decreased. By overexpressing PDE3B, we found that diosgenin inhibited the proliferation, migration, and inflammatory response of RA synovial cells by downregulating PDE3B. Diosgenin can inhibit excessive proliferation and inflammatory response of synovial fibroblasts by targeting PDE3B.
- Published
- 2021
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