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Ishige sinicola extract stimulates osteoblast proliferation and differentiation via the bone morphogenetic protein 2/runt-related gene 2 signalling pathway

  • Mihyang Kim , Jeong Hyeon Kang , Geun Hye Oh and Mi Hwa Park EMAIL logo
Published/Copyright: May 14, 2019
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Abstract

Osteoporosis is one of the most common bone diseases, occurring due to an imbalance between bone formation and bone resorption. The aim of this study was to investigate the effects of Ishige sinicola, a brown alga, on osteoblast differentiation through the activation of the bone morphogenetic protein 2 (BMP-2)/runt-related transcription factor 2 (Runx2) signalling pathway in MC3T3-E1 cells. A cell proliferation assay, alkaline phosphatase (ALP) activity assay, alizarin red staining, and expression analysis of osteoblastic genes were carried out to assess MC3T3-E1 cell proliferation and osteoblastic differentiation. We found that I. sinicola extract (ISE) increased cell proliferation in a dose-dependent manner. Ishige sinicola extract markedly promoted ALP activity and mineralization. Alizarin red S staining demonstrated that ISE treatment tended to increase extracellular matrix calcium accumulation. Moreover, ISE up-regulated the osteoprotegerin/receptor activator of nuclear factor κB ligand ratio. Ishige sinicola extract also increased the protein expression levels of type 1 collagen, ALP, osteocalcin, osterix, BMP-2, and Runx2. Therefore, ISE showed potential in stimulating osteoblastic bone formation, and it might be useful for the prevention and treatment of osteoporosis.

Award Identifier / Grant number: 2016R1D1A1B03935711

Funding statement: This work was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education (Funder Id: http://dx.doi.org/10.13039/501100003725, grant 2016R1D1A1B03935711).

  1. Author disclosure statement: The authors declare that there is no conflict of interest.

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Received: 2018-03-20
Revised: 2019-01-07
Accepted: 2019-04-16
Published Online: 2019-05-14
Published in Print: 2019-07-26

©2019 Walter de Gruyter GmbH, Berlin/Boston

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