骨溶解
骨吸收
破骨细胞
兰克尔
NF-κB
化学
MAPK/ERK通路
癌症研究
体内
细胞生物学
免疫印迹
信号转导
体外
受体
内科学
医学
牙科
生物化学
生物
基因
激活剂(遗传学)
生物技术
作者
Shijie Liao,Fangmin Song,Wenyu Feng,Xiaofei Ding,Jun Yao,Hui-jie Song,Yun Liu,Shiting Ma,Ziyi Wang,Xiaofeng Lin,Jiake Xu,Jinmin Zhao,Qian Liu
摘要
Prosthesis loosening is a highly troublesome clinical problem following total joint arthroplasty. Wear-particle-induced osteoclastogenesis has been shown to be the primary cause of periprosthetic osteolysis that eventually leads to aseptic prosthesis loosening. Therefore, inhibiting osteoclastogenesis is a promising strategy to control periprosthetic osteolysis. The possible mechanism of action of rhoifolin on osteoclastogenesis and titanium particle-induced calvarial osteolysis was examined in this study. The in vitro study showed that rhoifolin could strongly suppress the receptor activators of nuclear factor-κB (NF-κB) ligand-stimulated osteoclastogenesis, hydroxyapatite resorption, F-actin formation, and the gene expression of osteoclast-related genes. Western blot analysis illustrated that rhoifolin could attenuate the NF-κB and mitogen-activated protein kinase pathways, and the expression of transcriptional factors nuclear factor of activated T cells 1 (NFATc1) and c-Fos. Further studies indicated that rhoifolin inhibited p65 translocation to the nucleus and the activity of NFATc1 and NF-κB rhoifolin could decrease the number of tartrate-resistant acid phosphate-positive osteoclasts and titanium particle-induced C57 mouse calvarial bone loss in vivo. In conclusion, our results suggest that rhoifolin can ameliorate the osteoclasts-stimulated osteolysis, and may be a potential agent for the treatment of prosthesis loosening.
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