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Int. J. Mol. Sci. 2014, 15(12), 21913-21934; doi:10.3390/ijms151221913

The Inhibition of RANKL-Induced Osteoclastogenesis through the Suppression of p38 Signaling Pathway by Naringenin and Attenuation of Titanium-Particle-Induced Osteolysis

1
Shanghai Key Laboratory of Orthopedic Implants, Department of Orthopedics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
2
Department of Orthopedics, Hunan Provincial Tumor Hospital and Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha 410013, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 24 September 2014 / Revised: 30 October 2014 / Accepted: 24 November 2014 / Published: 28 November 2014
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

The aim of this study was to assess the effect of naringenin on osteoclastogenesis and titanium particle-induced osteolysis. Osteolysis from wear-induced particles and aseptic loosening are the most frequent late complications of total joint arthroplasty leading to revision of the prosthesis. Osteolysis during aseptic loosening is most likely due to increased bone resorption by osteoclasts. Through in vitro studies, we demonstrated that naringenin, a naturally occurring flavanone in grapefruit and tomatoes, exerts potent inhibitory effects on the ligand of the receptor activator of nuclear factor-κB (RANKL)-induced osteoclastogenesis and revealed that the mechanism of action of naringenin, which inhibited osteoclastogenesis by suppression of the p38 signaling pathway. Through in vivo studies, we proved that naringenin attenuated titanium particle-induced osteolysis in a mouse calvarial model. In general, we demonstrated that naringenin inhibited osteoclastogenesis via suppression of p38 signaling in vitro and attenuated titanium particle-induced osteolysis in vivo. This study also suggested that naringenin has significant potential for the treatment of osteolysis-related diseases caused by excessive osteoclast formation and activity. View Full-Text
Keywords: naringenin; osteolysis; osteoclast; p38 signaling; NFATc1 naringenin; osteolysis; osteoclast; p38 signaling; NFATc1
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Wang, W.; Wu, C.; Tian, B.; Liu, X.; Zhai, Z.; Qu, X.; Jiang, C.; Ouyang, Z.; Mao, Y.; Tang, T.; Qin, A.; Zhu, Z. The Inhibition of RANKL-Induced Osteoclastogenesis through the Suppression of p38 Signaling Pathway by Naringenin and Attenuation of Titanium-Particle-Induced Osteolysis. Int. J. Mol. Sci. 2014, 15, 21913-21934.

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