The novel isoflavone derivatives inhibit RANKL-induced osteoclast formation

Chih Hsin Tang, Chih Shiang Chang, Tzu Wei Tan, Shan Chi Liu, Ju Fang Liu

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)


Isoflavones are compounds structurally similar to the mammalian estrogens and have received considerable attention for their preventive actions on bone loss. Here, we synthesized the novel isoflavone derivatives and examined their activities in bone cells. We found that the novel isoflavone derivatives markedly inhibited the receptor activator of nuclear factor kappa B ligand (RANKL) plus macrophage colony stimulating factor (M-CSF)-induced osteoclastic differentiation from bone marrow stromal cells and RAW264.7 macrophage cells. Treatment of RAW264.7 macrophages with RANKL-induced extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinase (JNK) phosphorylation. However, RANKL-induced p38 and JNK but not ERK phosphorylation was attenuated by isoflavone derivatives. Furthermore, RANKL-mediated increase of p65 phosphorylation at Ser536, NF-κB-specific DNA-protein complex formation and κB-luciferase activity was inhibited by isoflavone derivatives. On the other hand, isoflavone derivatives did not affect the cell proliferation and differentiation of human cultured osteoblasts. Our data suggest that the novel isoflavone derivatives inhibit osteoclastogenesis from bone marrow stromal cells and macrophage cells via attenuation of RANKL-induced p38, JNK and NF-κB activation.

Original languageEnglish
Pages (from-to)59-66
Number of pages8
JournalEuropean Journal of Pharmacology
Issue number1-3
Publication statusPublished - Dec 1 2010


  • Chinese herb
  • Isoflavones
  • Osteoclast
  • Osteoporosis

ASJC Scopus subject areas

  • Pharmacology


Dive into the research topics of 'The novel isoflavone derivatives inhibit RANKL-induced osteoclast formation'. Together they form a unique fingerprint.

Cite this