Scutellarein inhibits RANKL-induced osteoclast formation in vitro and prevents LPS-induced bone loss in vivo

Fangsheng Fu, Siyuan Shao, Ziyi Wang, Fangming Song, Xixi Lin, Jiaxin Ding, Chen Li, Zuoxing Wu, Kai Li, Yu Xiao, Yiji Su, Jinmin Zhao, Qian Liu, Jiake Xu

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Abstract

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 as Ctsk9, Mmp9, Acp5, and Atp6v0d2. 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.

Original languageEnglish
Pages (from-to)11951-11959
Number of pages9
JournalJournal of Cellular Physiology
Volume234
Issue number7
DOIs
Publication statusPublished - 1 Jul 2019

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