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Sulforaphane Inhibits Osteoclastogenesis by Inhibiting Nuclear Factor-κB  

Kim, Soo-Jin (Department of Biological Sciences, and Immunomodulation Research Center, University of Ulsan)
Kang, So-Young (Department of Biological Sciences, and Immunomodulation Research Center, University of Ulsan)
Shin, Hyun-Hee (Department of Biological Sciences, and Immunomodulation Research Center, University of Ulsan)
Choi, Hye-Seon (Department of Biological Sciences, and Immunomodulation Research Center, University of Ulsan)
Abstract
We show that sulforaphane inhibits osteoclastogenesis in the presence of macrophage colony-stimulating factor (M-CSF) and receptor for activation of nuclear factor-${\kappa}B$ ligand (RANKL) in osteoclast (OC) precursors. Sulforaphane, an aliphatic isothiocyanate, is a known cancer chemo-preventative agent with anti-oxidative properties. Nuclear factor-${\kappa}B$ (NF-${\kappa}B$) is a critical transcription factor in RANKL-induced osteoclastogenesis, and electrophoretic mobility shift assays (EMSAs) and assay of NF-${\kappa}B$-mediated secreted alkaline phosphatase (SEAP) revealed that sulforaphane selectively inhibited NF-${\kappa}B$ activation induced by RANKL. Inhibition may involve interaction of sulforaphane with thiol groups, since it was prevented by reducing agents.
Keywords
Bone Marrow-derived Macrophages; NF-${\kappa}B$; Osteoclastogenesis; RANKL; Sulforaphane; Thiol;
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