Fermented Oyster Extract Prevents Ovariectomy-Induced Bone Loss and Suppresses Osteoclastogenesis

There is growing interest in bioactive substances from marine organisms for their potential use against diverse human diseases. Osteoporosis is a skeletal disorder associated with bone loss primarily occurring through enhanced osteoclast differentiation and resorption. Recently, we reported the anti...

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Bibliographic Details
Published in:Nutrients
Main Authors: Hye Jung Ihn, Ju Ang Kim, Soomin Lim, Sang-Hyeon Nam, So Hyeon Hwang, Jiwon Lim, Gi-Young Kim, Yung Hyun Choi, You-Jin Jeon, Bae-Jin Lee, Jong-Sup Bae, Yeo Hyang Kim, Eui Kyun Park
Format: Article in Journal/Newspaper
Language:English
Published: MDPI AG 2019
Subjects:
osteoclast
ovariectomy
fermented oyster extract
bone loss
Nutrition. Foods and food supply
TX341-641
Pacific
Crassostrea gigas
Pacific oyster
Online Access:https://doi.org/10.3390/nu11061392
https://doaj.org/article/575931f1d8044ead9c4267d2cafd2012
Description
Summary:There is growing interest in bioactive substances from marine organisms for their potential use against diverse human diseases. Osteoporosis is a skeletal disorder associated with bone loss primarily occurring through enhanced osteoclast differentiation and resorption. Recently, we reported the anti-osteoclastogenic activity of fermented Pacific oyster ( Crassostrea gigas ) extract (FO) in vitro. The present study focused on investigating the anti-osteoporotic efficacy of FO in bone loss prevention in an experimental animal model of osteoporosis and elucidating the mechanism underlying its effects. Oral administration of FO significantly decreased ovariectomy-induced osteoclast formation and prevented bone loss, with reduced serum levels of bone turnover biomarkers including osteocalcin and C-terminal telopeptide fragment of type I collagen C-terminus (CTX). FO significantly suppressed receptor activator of nuclear factor-κB ligand (RANKL)-induced differentiation of bone marrow-derived macrophages (BMMs) into osteoclasts and attenuated the induction of osteoclast-specific genes required for osteoclastogenesis and bone resorption. Furthermore, FO inhibited RANKL-mediated IκBα and p65 phosphorylation in BMMs. Taken together, these results demonstrate that FO effectively suppresses osteoclastogenesis in vivo and in vitro, and that FO can be considered as a potential therapeutic option for the treatment of osteoporosis and osteoclast-mediated skeletal diseases.

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