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Luteoloside prevents lipopolysaccharide-induced osteolysis and suppresses RANKL-induced osteoclastogenesis through attenuating RANKL signaling cascades.

Authors
  • Song, Fangming1, 2
  • Wei, Chengming1
  • Zhou, Lin2
  • Qin, An3
  • Yang, Mingli2
  • Tickner, Jennifer2
  • Huang, Yuanjiao4
  • Zhao, Jinmin1, 5
  • Xu, Jiake1, 2
  • 1 Research Centre for Regenerative Medicine, Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi, China. , (China)
  • 2 School of Biomedical Sciences, The University of Western Australia, Perth, Western Australia, Australia. , (Australia)
  • 3 Department of Orthopaedics Surgery, Shanghai Key Laboratory of Orthopaedic Implant, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. , (China)
  • 4 Medical Scientific Research Center, Guangxi Medical University, Nanning, Guangxi, China. , (China)
  • 5 Department of Orthopaedic Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China. , (China)
Type
Published Article
Journal
Journal of Cellular Physiology
Publisher
Wiley (John Wiley & Sons)
Publication Date
Feb 01, 2018
Volume
233
Issue
2
Pages
1723–1735
Identifiers
DOI: 10.1002/jcp.26084
PMID: 28681916
Source
Medline
Keywords
License
Unknown

Abstract

Bone destruction or osteolysis marked by excessive osteoclastic bone resorption is a very common medical condition. Identification of agents that can effectively suppress excessive osteoclast formation and function is crucial for prevention and treatment of osteolytic conditions such as periprosthetic joint infection and periprosthetic loosening. Luteoloside, a flavonoid, is a natural bioactive compound with anti-inflammation and anti-tumor properties. However, the effect of Luteoloside on inflammation-induced osteolysis is unknown. Here, we found that Luteoloside exhibited a strong inhibitory effect on lipopolysaccharide (LPS)-induced osteolysis in vivo. In addition, Luteoloside suppressed RANKL-induced osteoclast differentiation and abrogated bone resorption in a dose-dependent manner. Further, we found that the anti-osteoclastic and anti-resorptive actions of Luteoloside are mediated via blocking NFATc1 activity and the attenuation of RANKL-mediated Ca2+ signaling as well as NF-κB and MAPK pathways. Taken together, this study shows that Luteoloside may be a potential therapeutic agent for osteolytic bone diseases associated with abnormal osteoclast formation and function in inflammatory conditions.

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