Taxifolin Inhibits Receptor Activator of NF-κB Ligand-Induced Osteoclastogenesis of Human Bone Marrow-Derived Macrophages in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo

Taxifolin Inhibits Receptor Activator of NF-κB Ligand-Induced Osteoclastogenesis of Human Bone Marrow-Derived Macrophages in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo
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紫杉叶素在体外抑制 NF-κB 配体诱导的人骨髓源性巨噬细胞破骨细胞形成的受体激活剂,并在体内防止脂多糖诱导的骨丢失

DOI:
10.1159/000495254
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发表时间:
2018-12
期刊:
影响因子:
3.1
通讯作者:
Ming-Xing Tang
Ming-Xing Tang
中科院分区:
医学4区
文献类型:
--
作者:
Hong-Qi Zhang;Yun-Jia Wang;Guan-Teng Yang;Qi-Le Gao;Ming-Xing Tang

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It has been reported that taxifolin inhibit osteoclastogenesis in RAW264. 7 cells. In our research, the inhibition effects of taxifolin on the osteoclastogenesis of human bone marrow-derived macrophages (BMMs) induced by receptor activator of NF-κB ligand (RANKL) as well as the protection effects in lipopolysaccharide-induced bone lysis mouse model have been demonstrated. In vitro, taxifolin inhibited RANKL-induced osteoclast differentiation of human BMMs without cytotoxicity. Moreover, taxifolin significantly suppressed RANKL-induced gene expression, including tartrate-resistant acid phosphatase, matrix metalloproteinase-9 nuclear factor of activated T cells 1 and cathepsin K, and F-actin ring formation. Further studies showed that taxifolin inhibit osteoclastogenesis via the suppression of the NF-κB signaling pathway. In vivo, taxifolin prevented bone loss in mouse calvarial osteolysis model. In conclusion, the results suggested that taxifolin has a therapeutic potential for osteoclastogenesis-related diseases such as osteoporosis, osteolysis, and rheumatoid arthritis.
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