Hederagenin inhibits proliferation, angiogenesis and inflammation of fibroblast-like synovial cells in rheumatoid arthritis.

Purpose: To determine the effect of Hederagenin (Hed) on rheumatoid arthritis (RA) in a cell model, and to elucidate the mechanism of action of Hed. Methods: MTT, EDU, and Immunoblot assays were used to determine the effects of Hed on the viability of fibroblast-like synovial cells, while the effects of Hed on inflammation were examined by enzymelinked immunosorbent assay (ELISA) and immunoblot assay. The influence of Hed on cell motility angiogenesis was evaluated by Transwell and tube formation assays, while immunoblot analysis was used to determine the mechanism of action of Hed. Results: Hed inhibited the viability of RA-FLS cells and suppressed the inflammation of RA-FLS cells (p < 0.05). Furthermore, Hed suppressed the migration and angiogenesis of RA-FLSl cells, as well as regulated MAPK pathway (p < 0.05). Conclusion: Hed inhibits the proliferation, angiogenesis and inflammation of fibroblast-like synovial cells in RA by regulating MAPK pathway. Therefore, Hed is a drug for the treatment of RA, However, in vivo studies to validate these findings are recommended. [ABSTRACT FROM AUTHOR]