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

• Published in: Nutrients
• Main Authors: Ihn, Hye Jung, Kim, Ju Ang, Lim, Soomin, Nam, Sang-Hyeon, Hwang, So Hyeon, Lim, Jiwon, Kim, Gi-Young, Choi, Yung Hyun, Jeon, You-Jin, Lee, Bae-Jin, Bae, Jong-Sup, Kim, Yeo Hyang, Park, Eui Kyun
• Format: Text
• Language: English
• Published: MDPI 2019
• Subjects: Article; Pacific; Crassostrea gigas; Pacific oyster
• Online Access: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627411/; http://www.ncbi.nlm.nih.gov/pubmed/31234292; https://doi.org/10.3390/nu11061392

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.