Osthole inhibits osteoclasts formation and bone resorption by regulating NF-κB signaling and NFATc1 activations stimulated by RANKL

J Cell Biochem. 2019 Sep;120(9):16052-16061. doi: 10.1002/jcb.28886. Epub 2019 May 13.

Abstract

Chinese herbal medicine Fructus Cnidii has an outstanding effect on chronic lumbar pain and impotence, also has been used against osteoporosis with high frequency. Yet, the mechanisms of osthole, a derivative of Fructus Cnidii, on osteoclasts remains barely known. In this study, it was found out that osthole (10-6 mol/L, 10-5 mol/L) had the influence of inhibiting osteoclast formation and bone resorptive activities induced by receptor activator of nuclear factor κB ligand (RANKL), rather than affecting the viability of osteoclast-like cells. Furthermore, osthole could also inhibit the messenger RNA expressions of c-Src, tartrate-resistant acid phosphatase, β3-Integrin, matrix metallopeptidase 9, and cathepsin K. The results of the mechanistic study indicated that osthole regulated the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and nuclear factor-κB (NF-κB) activations following the RANKL stimulation. These findings suggested that the inhibitory effects of osthole were associated with restraining the activations of NFATc1 and NF-κB induced by RANKL. Thus osthole can be used as a potential treatment for abnormal bone-resorption related diseases.

Keywords: nuclear factor of activated T-cells cytoplasmic 1; nuclear factor-κB signaling pathway; osteoclasts; osteoporosis; osthole.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone Resorption / drug therapy
  • Bone Resorption / genetics
  • Bone Resorption / metabolism*
  • Cell Differentiation / drug effects
  • Coumarins / pharmacology*
  • Gene Expression Regulation / drug effects
  • Mice
  • NF-kappa B / metabolism
  • NFATC Transcription Factors / genetics
  • NFATC Transcription Factors / metabolism*
  • Osteoclasts / cytology*
  • Osteoclasts / drug effects
  • Osteoclasts / metabolism
  • RANK Ligand / genetics
  • RANK Ligand / metabolism*
  • RAW 264.7 Cells
  • Signal Transduction / drug effects

Substances

  • Coumarins
  • NF-kappa B
  • NFATC Transcription Factors
  • Nfatc1 protein, mouse
  • RANK Ligand
  • Tnfsf11 protein, mouse
  • osthol