magnosalin and Arthritis--Rheumatoid

This study was undertaken to examine the effects of magnosalin, a compound isolated from 'Shin-i' (Flos magnoliae) on proliferation of synovial cells isolated from MRL/1pr and collagen-induced arthritis (CIA) mice, and rheumatoid arthritis (RA) patients. Magnosalin (2.39-23.9 microM) inhibited 5% fetal bovine serum (FBS)-stimulated [3H]-thymidine incorporation into the synovial cells in the MRL/1pr mice. The effect of magnosalin was greater than that of hydrocortisone, bucillamine and magnoshinin (another compound from 'Shin-i'), but weaker than that of corticosterone. The effects of magnosalin for FBS-induced thymidine incorporation into the cells of the CIA mice and the RA patients were significantly greater than those in the corresponding control mice and osteoarthritis patients. Interleukin (IL)-1alpha increased the incorporation of thymidine into the synovial cells in the C57BL/6J mice to a greater degree than did basic fibroblast growth factor (bFGF) or platelet-derived growth factor BB-homodimer (PDGF-BB). The inhibitory effect of magnosalin on the submaximal action of IL-1alpha was significantly greater than that of bFGF, PDGF-BB or FBS. These results offer evidence that magnosalin suppresses the proliferation of synovial cells in RA models by inhibiting IL-1alpha-stimulated action.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antirheumatic Agents; Arthritis, Rheumatoid; Cell Division; Cyclobutanes; Cytokines; Interleukin-1; Male; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; Mice, Inbred MRL lpr; Synovial Membrane; Thymidine