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Inhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression
BACKGROUND: Schisandra chinenesis (SC) has been reported to have ameliorative effect on osteoporosis. However, the mechanisms underlying the anti-osteoporosis activity of SC have not been clearly elucidated. In the present study, we determined the effects of SC on The receptor activator of NF-kB lig...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6167898/ https://www.ncbi.nlm.nih.gov/pubmed/30285722 http://dx.doi.org/10.1186/s12906-018-2331-5 |
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author | Kim, Eun-Jung Lee, Haesu Kim, Mi Hye Yang, Woong Mo |
author_facet | Kim, Eun-Jung Lee, Haesu Kim, Mi Hye Yang, Woong Mo |
author_sort | Kim, Eun-Jung |
collection | PubMed |
description | BACKGROUND: Schisandra chinenesis (SC) has been reported to have ameliorative effect on osteoporosis. However, the mechanisms underlying the anti-osteoporosis activity of SC have not been clearly elucidated. In the present study, we determined the effects of SC on The receptor activator of NF-kB ligand (RANKL)-induced osteoclastogenesis and its potential mechanism. METHODS: Raw 264.7 cells were treated with 0.6, 6 and 60 μg/mL SC in the presence of 100 ng/mL RANKL for 7 days. RANKL-induced osteoclast formation was analyzed by tartrate resistant acid phosphatase (TRAP) staining. The osteoclast differentiation-related factors were confirmed along with TNF-α. RESULTS: SC inhibits the RANKL-induced osteoclast differentiation in dose-dependent manner within non-toxic concentrations. The supernatant concentrations of TNF-α were significantly decreased by SC treatment. In addition, osteoclastogenesis-related factors, TRAP6 and NF-κB, were markedly decreased by SC in RANKL-induced osteoclasts. Mechanistically, SC reduced the RANKL-triggered NFATc1 and c-fos expressions. CONCLUSIONS: Taken together, our data suggest that SC can modulate bone metabolism by suppressing RANKL-induced osteoclast differentiation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12906-018-2331-5) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6167898 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-61678982018-10-09 Inhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression Kim, Eun-Jung Lee, Haesu Kim, Mi Hye Yang, Woong Mo BMC Complement Altern Med Research Article BACKGROUND: Schisandra chinenesis (SC) has been reported to have ameliorative effect on osteoporosis. However, the mechanisms underlying the anti-osteoporosis activity of SC have not been clearly elucidated. In the present study, we determined the effects of SC on The receptor activator of NF-kB ligand (RANKL)-induced osteoclastogenesis and its potential mechanism. METHODS: Raw 264.7 cells were treated with 0.6, 6 and 60 μg/mL SC in the presence of 100 ng/mL RANKL for 7 days. RANKL-induced osteoclast formation was analyzed by tartrate resistant acid phosphatase (TRAP) staining. The osteoclast differentiation-related factors were confirmed along with TNF-α. RESULTS: SC inhibits the RANKL-induced osteoclast differentiation in dose-dependent manner within non-toxic concentrations. The supernatant concentrations of TNF-α were significantly decreased by SC treatment. In addition, osteoclastogenesis-related factors, TRAP6 and NF-κB, were markedly decreased by SC in RANKL-induced osteoclasts. Mechanistically, SC reduced the RANKL-triggered NFATc1 and c-fos expressions. CONCLUSIONS: Taken together, our data suggest that SC can modulate bone metabolism by suppressing RANKL-induced osteoclast differentiation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12906-018-2331-5) contains supplementary material, which is available to authorized users. BioMed Central 2018-10-01 /pmc/articles/PMC6167898/ /pubmed/30285722 http://dx.doi.org/10.1186/s12906-018-2331-5 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Kim, Eun-Jung Lee, Haesu Kim, Mi Hye Yang, Woong Mo Inhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression |
title | Inhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression |
title_full | Inhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression |
title_fullStr | Inhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression |
title_full_unstemmed | Inhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression |
title_short | Inhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression |
title_sort | inhibition of rankl-stimulated osteoclast differentiation by schisandra chinensis through down-regulation of nfatc1 and c-fos expression |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6167898/ https://www.ncbi.nlm.nih.gov/pubmed/30285722 http://dx.doi.org/10.1186/s12906-018-2331-5 |
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