Inhibitory effects of biochanin A on titanium particle-induced osteoclast activation and inflammatory bone resorption via NF-κB and MAPK pathways

被引：25
|
作者：
Liao, Shijie [1 ,2 ]
Feng, Wenyu [1 ,2 ]
Liu, Yun [1 ,3 ]
Wang, Ziyi [3 ]
Ding, Xiaofei [1 ,2 ]
Song, Fangming [2 ,3 ]
Lin, Xixi [2 ]
Song, Huijie [4 ]
Anil, K. C. [1 ]
Su, Yuangang [2 ]
Liang, Jiamin [2 ]
Xu, Jiake [2 ,3 ]
Liu, Qian [1 ,2 ]
Zhao, Jinmin [1 ,2 ]
机构：
[1] Guangxi Med Univ, Dept Orthopaed, Affiliated Hosp 1, Nanning 530021, Guangxi, Peoples R China
[2] Guangxi Med Univ, Res Ctr Regenerat Med, Guangxi Key Lab Regenerat Med, Nanning, Guangxi, Peoples R China
[3] Univ Western Australia, Sch Biomed Sci, Perth, WA, Australia
[4] Guangxi Univ Chinese Med, Dept Anesthesiol, Affliated Hosp 1, Nanning, Guangxi, Peoples R China
来源：
JOURNAL OF CELLULAR PHYSIOLOGY | 2021年 / 236卷 / 02期
基金：
中国国家自然科学基金;
关键词：
biochanin A; inflammatory; MAPK; NF-kappa B; osteoclast; INDUCED OSTEOLYSIS; DIFFERENTIATION; SUPPRESSION; DENOSUMAB; SURVIVAL; DISEASE; GROWTH; ROLES;
D O I：
10.1002/jcp.29948
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Revision operations have become a new issue after successful artificial joint replacements, and periprosthetic osteolysis leading to prosthetic loosening is the main cause of why the overactivation of osteoclasts (OCs) plays an important role. The effect of biochanin A (BCA) has been examined in osteoporosis, but no study on the role of BCA in prosthetic loosening osteolysis has been conducted yet. In this study, we utilised enzyme-linked immunosorbent assay, computed tomography imaging, and histological analysis. Results showed that BCA downregulated the secretion levels of tumor necrosis factor-alpha, interleukin-1 alpha (IL-1 alpha), and IL-1 beta to suppress inflammatory responses. The secretion levels of receptor-activated nuclear factor-kappa B ligand, CTX-1, and osteoclast-associated receptor as well as Ti-induced osteolysis were also reduced. BCA effectively inhibited osteoclastogenesis and suppressed hydroxyapatite resorption by downregulating OC-related genes in vitro. Analysis of mechanisms indicated that BCA inhibited the signalling pathways of mitogen-activated protein kinase (P38, extracellular signal-regulated kinase, and c-JUN N-terminal kinase) and nuclear factor-kappa B (inhibitor kappa B-alpha and P65), thereby downregulating the expression of nuclear factor of activated T cell 1 and c-Fos. In conclusion, BCA may be an alternative choice for the prevention of prosthetic loosening caused by OCs.
引用
收藏
页码：1432 / 1444
页数：13
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