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

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 ost...

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Veröffentlicht in:Journal of cellular physiology 2021-02, Vol.236 (2), p.1432-1444
Hauptverfasser: Liao, Shijie, Feng, Wenyu, Liu, Yun, Wang, Ziyi, Ding, Xiaofei, Song, Fangming, Lin, Xixi, Song, Huijie, KC, Anil, Su, Yuangang, Liang, Jiamin, Xu, Jiake, Liu, Qian, Zhao, Jinmin
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container_end_page 1444
container_issue 2
container_start_page 1432
container_title Journal of cellular physiology
container_volume 236
creator Liao, Shijie
Feng, Wenyu
Liu, Yun
Wang, Ziyi
Ding, Xiaofei
Song, Fangming
Lin, Xixi
Song, Huijie
KC, Anil
Su, Yuangang
Liang, Jiamin
Xu, Jiake
Liu, Qian
Zhao, Jinmin
description 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. This is a valuable study on osteoclasts, which verified the effectiveness of traditional Chinese medicine monomer.
doi_str_mv 10.1002/jcp.29948
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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. 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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. 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subjects Artificial joints
Biochanin A
Biomedical materials
Bone resorption
Bone surgery
Collagen
Computed tomography
Hydroxyapatite
Inflammation
inflammatory
Interleukins
JNK protein
Kinases
Loosening
Lymphocytes
MAP kinase
MAPK
NF‐κB
osteoclast
Osteoclastogenesis
Osteoclasts
Osteolysis
Osteoporosis
Prostheses
Protein kinase
Receptors
Signal transduction
Surgical implants
Titanium
title Inhibitory effects of biochanin A on titanium particle‐induced osteoclast activation and inflammatory bone resorption via NF‐κB and MAPK pathways
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