20(S)-Protopanaxadiol Inhibits Titanium Particle-Induced Inflammatory Osteolysis and RANKL-Mediated Osteoclastogenesis via MAPK and NF-κB Signaling Pathways

被引：15

作者：

Pan, Chenhao ^{[1
]}

Shan, Haojie ^{[1
]}

Wu, Tianyi ^{[1
]}

Liu, Wei ^{[1
]}

Lin, Yiwei ^{[1
]}

Xia, Wenyang ^{[1
]}

Wang, Feng ^{[2
]}

Zhou, Zubin ^{[1
]}

Yu, Xiaowei ^{[1
,2
]}

机构：

[1] Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Dept Orthoped Surg, Shanghai, Peoples R China

[2] Shanghai Univ Med & Hlth Sci, Shanghai Peoples Hosp 6, Dept Orthoped Surg, East Campus, Shanghai, Peoples R China

来源：

FRONTIERS IN PHARMACOLOGY | 2019年 / 9卷

基金：

中国国家自然科学基金;

关键词：

inflammation; bone resorption; MAPK signaling; NF-kappa B signaling; 20(S)-protopanaxadiol; WEAR DEBRIS; C-FOS; COMPOUND K; TOTAL HIP; DIFFERENTIATION; SUPPRESSION; ACTIVATION; NFATC1; KINASE; MACROPHAGES;

D O I：

10.3389/fphar.2018.01538

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Osteolysis is a principal reason for arthroplasty failure like aseptic loosening induced by Titanium (Ti) particle. It is a challenge for orthopedic surgeons. Recent researches show that 20(S)-protopanaxadiol can inhibit inflammatory cytokine release in vitro. This study aims to assess the effect of 20(S)-protopanaxadiol on Ti particle-induced osteolysis and RANKL-mediated osteoclastogenesis. Micro-CT and histological analysis in vivo indicated the inhibitory effects of 20(S)-protopanaxadiol on osteoclastogenesis and the excretion of inflammatory cytokines. Next, we demonstrated that 20(S)-protopanaxadiol inhibited osteoclast differentiation, bone resorption area, and F-actin ring formation in a dose-dependent manner. Moreover, mechanistic studies suggested that the suppression of MAPK and NF-kappa B signaling pathways were found to mediate the inhibitory effects of 20(S)-protopanaxadiol. In conclusion, 20(S)-protopanaxadiol may suppress osteoclastogenesis in a dose-dependent manner and it could be a potential treatment of Ti particle-induced osteolysis.

引用

页数：12

共 52 条

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