Ganomycin I from Ganoderma lucidum attenuates RANKL-mediated osteoclastogenesis by inhibiting MAPKs and NFATc1

摘要: Background Many bone-related diseases such as osteoporosis and rheumatoid arthritis are commonly associated with excessive activity of the osteoclast. Ganomycin I (GMI), a meroterpenoid isolated from Vietnamese mushroom Ganoderma lucidum, possesses variety beneficial effects on human health. However, its impact underlying mechanism osteoclastogenesis remain unclear. In present study, we investigated effect GMI RANKL-induced osteoclast formation in mouse BMMs RAW264.7 cells. Methods or cells were treated followed by an evaluation cell viability, differentiation, actin-ring formation, resorption pits activity. Effects phosphorylation MAPKs well expression levels NFATc1 c-Fos evaluated Western blot analysis. Expression marker genes analysis reverse transcription-qPCR. Results significantly inhibited differentiation decreasing number osteoclasts, bone dose-dependent manner without affecting viability. At molecular level, ERK, JNK, p38 MAPKs, NFATc1, which known to be crucial transcription factors for formation. addition, decreased specific including c-Src, CtsK, TRAP, MMP-9, OSCAR, DC-STAMP RANKL-stimulated BMMs. Conclusion Our findings suggest that can attenuate suppressing RANKL-mediated signaling pathways anti-osteoclastogenic may extend our understanding mechanisms biological activities pharmacological use G. lucidum traditional anti-osteoporotic medicine.