Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/68841
標題: The novel isoflavone derivatives inhibit RANKL-induced osteoclast formation
作者: Tang, C.H.
Chang, C.S.
Tan, T.W.
Liu, S.C.
Liu, J.F.
關鍵字: Isoflavones;Osteoclast;Osteoporosis;RANKL;Chinese herb;nf-kappa-b;stimulating factor-i;cell-surface form;bone loss;activation;kinase;genistein;protein;rats;expression
Project: European Journal of Pharmacology
期刊/報告no:: European Journal of Pharmacology, Volume 648, Issue 1-3, Page(s) 59-66.
摘要: 
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 Ser(536), NF-kappa B-specific DNA-protein complex formation and kappa B-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-kappa B activation. (C) 2010 Elsevier B.V. All rights reserved.
URI: http://hdl.handle.net/11455/68841
ISSN: 0014-2999
DOI: 10.1016/j.ejphar.2010.08.052
Appears in Collections:期刊論文

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