Scutellarein inhibits RANKL-induced osteoclast formation in vitro and prevents LPS-induced bone loss in vivo.
Fangsheng FuSiyuan ShaoZiyi WangFangming SongXixi LinJiaxin DingChen LiZuoxing WuKai LiYu XiaoYiji SuJinmin ZhaoQian LiuJiake XuPublished in: Journal of cellular physiology (2018)
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.
Keyphrases
- bone loss
- lps induced
- gene expression
- oxidative stress
- inflammatory response
- bone mineral density
- diabetic rats
- high glucose
- rheumatoid arthritis
- postmenopausal women
- emergency department
- dna methylation
- total hip
- cell proliferation
- combination therapy
- pi k akt
- total hip arthroplasty
- single cell
- mouse model
- smoking cessation
- induced apoptosis
- bone regeneration