Scutellarein inhibits RANKL-induced osteoclast formation in vitro and prevents LPS-induced bone loss in vivo.
Scutellarein inhibits RANKL-induced osteoclast formation in vitro and prevents LPS-induced bone loss in vivo.
复制标题
Scutellarein 在体外抑制 RANKL 诱导的破骨细胞形成,并在体内防止 LPS 诱导的骨质流失。
DOI:
10.1002/jcp.27888
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发表时间:
2018
影响因子:
5.6
通讯作者:
Xu Jiake
中科院分区:
文献类型:
--
作者:
Fu Fangsheng;Shao Siyuan;Wang Ziyi;Song Fangming;Lin Xixi;Ding Jiaxin;Li Chen;Wu Zuoxing;Li Kai;Xiao Yu;Su Yiji;Zhao Jinmin;Liu Qian;Xu Jiake
Osteoporosis, arthritis, Peget's disease, bone tumor, periprosthetic joint infection, and periprosthetic loosening have a common characteristic of osteolysis, which is characterized by the enhanced osteoclastic bone resorptive function. At present, the treatment target of these diseases is to interfere with osteoclastic formation and function. Scutellarein (Scu), a flavonoids compound, can inhibit the progress of tumor and inflammation. However, the role of Scu in inflammatory osteolysis isn’t elucidated clearly. Our study showed that Scu inhibited bone destruction induced by LPS in vivo and OC morphology and function induced by RANKL in vitro. Mechanistic studies revealed that Scu suppressed osteoclastic marker gene expression by RANKL‐induced, such asCtsk9,Mmp9,Acp5, andAtp6v0d2. In addition, we found that the inhibition effects of osteoclastogenesis and bone resorption function of Scu were mediated via attenuating NF‐κB and NFAT signaling pathways. In conclusion, the results showed that Scu may become a potential new drug for the treatment of inflammatory osteolysis.