Aconine

Aconine inhibits receptor activator of nuclear factor (NF)-κB ligand (RANKL)-induced NF-κB activation. IC50 & Target: NF-κB^[1] In Vitro: Treatment with Aconine significantly inhibits the RANKL-induced transcriptional activity of NF-κB in a dose-dependent manner. Aconine inhibits RANKL-induced osteoclast differentiation in RAW264.7 cells by suppressing the activation of NF-κB and NFATc1 and the expression of the cell-cell fusion molecule DC-STAMP. Aconine (0.125, 0.25 μM) does not affect the viability of RAW264.7 cells, but dose-dependently inhibits RANKL-induced osteoclast formation and bone resorptive activity. Aconine dose-dependently inhibits the RANKL-induced activation of NF-κB and NFATc1 in RAW264.7 cells, and subsequently reduces the expression of osteoclast-specific genes (c-Src, β3-Integrin, cathepsin K and MMP-9) and the expression of dendritic cell-specific transmembrane protein (DC-STAMP), which plays an important role in cell-cell fusion^[1].