9-Hydroxy-6,7-dimethoxydalbergiquinol inhibits osteoclast differentiation through down-regulation of Akt, c-Fos and NFATc1

Int Immunopharmacol. 2014 May;20(1):213-20. doi: 10.1016/j.intimp.2014.03.001. Epub 2014 Mar 14.

Abstract

Recently, natural plant-derived products have been recognized as one of the main sources for drug discovery and development in human disease. 9-Hydroxy-6,7-dimethoxydalbergiquinol (HDDQ) isolated from the heart wood of Dalbergia odorifera is widely used in oriental medicine, however, the pharmacological effect of HDDQ in osteoclast-associated diseases remains unknown. In this study, HDDQ dose-dependently inhibited the early stage of RANKL-mediated osteoclast differentiation in bone marrow macrophages (BMMs) without cytotoxicity. HDDQ strongly inhibited Akt phosphorylation in RANKL-stimulated BMMs and did not show any effects on p38, JNK, and IκB phosphorylation and IκB degradation. Interestingly, we found that HDDQ down-regulated the induction by RANKL of c-Fos protein by suppressing its translation. Also, ectopic overexpression of c-Fos and NFATc1 rescued the inhibition of osteoclast differentiation by HDDQ. Furthermore, the Akt/c-Fos/NFATc1-regulated expression of genes required for osteoclastogenesis, such as OSCAR and TRAP, was inhibited by HDDQ. These findings suggest that HDDQ prevents osteoclast differentiation via down-regulation of Akt, c-Fos, and NFATc1 signaling molecules, suggesting a potential therapeutic value of HDDQ for bone disorders associated with increased bone resorption.

Keywords: 9-Hydroxy-6,7-dimethoxydalbergiquinol; Osteoclasts; Osteoporosis; RANKL.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acid Phosphatase / genetics
  • Allyl Compounds / pharmacology*
  • Animals
  • Anisoles / pharmacology*
  • Bone Marrow Cells / cytology
  • Cell Differentiation / drug effects
  • Cells, Cultured
  • Isoenzymes / genetics
  • Macrophage Colony-Stimulating Factor / pharmacology
  • Macrophages / cytology
  • Macrophages / drug effects*
  • Macrophages / metabolism
  • Male
  • Mice, Inbred ICR
  • NFATC Transcription Factors / genetics
  • NFATC Transcription Factors / metabolism*
  • Osteoclasts / cytology
  • Osteoclasts / drug effects*
  • Osteoclasts / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-fos / metabolism*
  • RANK Ligand / pharmacology
  • Receptors, Cell Surface / genetics
  • Tartrate-Resistant Acid Phosphatase

Substances

  • 9-hydroxy-6,7-dimethoxydalbergiquinol
  • Allyl Compounds
  • Anisoles
  • Isoenzymes
  • NFATC Transcription Factors
  • Nfatc1 protein, mouse
  • Oscar protein, mouse
  • Proto-Oncogene Proteins c-fos
  • RANK Ligand
  • Receptors, Cell Surface
  • Macrophage Colony-Stimulating Factor
  • Proto-Oncogene Proteins c-akt
  • Acid Phosphatase
  • Acp5 protein, mouse
  • Tartrate-Resistant Acid Phosphatase