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

Shijie Liao, Wenyu Feng, Yun Liu, Ziyi Wang, Xiaofei Ding, Fangming Song, Xixi Lin, Huijie Song, K. C. Anil, Yuangang Su, Jiamin Liang, Jiake Xu, Qian Liu, Jinmin Zhao

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)

Abstract

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-α, interleukin-1α (IL-1α), and IL-1β to suppress inflammatory responses. The secretion levels of receptor-activated nuclear factor-κB 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-κB (inhibitor κB-α 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.

Original languageEnglish
Pages (from-to)1432-1444
Number of pages13
JournalJournal of Cellular Physiology
Volume236
Issue number2
DOIs
Publication statusPublished - Feb 2021

Fingerprint

Dive into the research topics of 'Inhibitory effects of biochanin A on titanium particle-induced osteoclast activation and inflammatory bone resorption via NF-κB and MAPK pathways'. Together they form a unique fingerprint.

Cite this