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Hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of BMSCs via activation of the NF‐κB pathway
Hyperoside, as an active compound, widely exists in a large number of Chinese herbal medicines and has been reported to possess anti‐inflammatory and diuretic properties. However, the effects and underlying mechanisms of hyperoside on periodontitis have not been previously reported. In this study, w...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7459408/ https://www.ncbi.nlm.nih.gov/pubmed/32687664 http://dx.doi.org/10.1002/2211-5463.12937 |
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author | Xu, Tao Wu, Xiao Zhou, Zhou Ye, Yu Yan, Chaoting Zhuge, Nanshan Yu, Jinhua |
author_facet | Xu, Tao Wu, Xiao Zhou, Zhou Ye, Yu Yan, Chaoting Zhuge, Nanshan Yu, Jinhua |
author_sort | Xu, Tao |
collection | PubMed |
description | Hyperoside, as an active compound, widely exists in a large number of Chinese herbal medicines and has been reported to possess anti‐inflammatory and diuretic properties. However, the effects and underlying mechanisms of hyperoside on periodontitis have not been previously reported. In this study, we found that hyperoside ameliorates symptoms of periodontitis in a rat model, with improvements in alveolar bone resorption, relief of inflammatory infiltration, increase in orderly arrangement of collagen fibers and increase of osteogenic differentiation. In addition, hyperoside promoted proliferation, up‐regulated EdU‐positive cells, decreased cell‐cycle distribution and increased the protein expression of Ki67 and PCNA in rat bone mesenchymal stem cells (rBMSCs), as revealed by Cell Counting Kit‐8, EdU, flow cytometry and western blot analysis. Moreover, hyperoside significantly promoted osteogenic differentiation, as shown by quantitative RT‐PCR, western blot and alizarin red staining assays. Furthermore, hyperoside activated the nuclear factor‐κB (NF‐κB) signaling pathway in rBMSCs, similar to the results observed in vivo. Finally, BMS345541, an inhibitor of the NF‐κB signaling pathway, could reverse the effects of hyperoside on the biological functions in rBMSCs. In conclusion, our results suggest that hyperoside has potential therapeutic properties against periodontitis via promotion of proliferation and osteogenic differentiation of rBMSCs via activation of the NF‐κB signaling pathway. |
format | Online Article Text |
id | pubmed-7459408 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-74594082020-09-03 Hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of BMSCs via activation of the NF‐κB pathway Xu, Tao Wu, Xiao Zhou, Zhou Ye, Yu Yan, Chaoting Zhuge, Nanshan Yu, Jinhua FEBS Open Bio Research Articles Hyperoside, as an active compound, widely exists in a large number of Chinese herbal medicines and has been reported to possess anti‐inflammatory and diuretic properties. However, the effects and underlying mechanisms of hyperoside on periodontitis have not been previously reported. In this study, we found that hyperoside ameliorates symptoms of periodontitis in a rat model, with improvements in alveolar bone resorption, relief of inflammatory infiltration, increase in orderly arrangement of collagen fibers and increase of osteogenic differentiation. In addition, hyperoside promoted proliferation, up‐regulated EdU‐positive cells, decreased cell‐cycle distribution and increased the protein expression of Ki67 and PCNA in rat bone mesenchymal stem cells (rBMSCs), as revealed by Cell Counting Kit‐8, EdU, flow cytometry and western blot analysis. Moreover, hyperoside significantly promoted osteogenic differentiation, as shown by quantitative RT‐PCR, western blot and alizarin red staining assays. Furthermore, hyperoside activated the nuclear factor‐κB (NF‐κB) signaling pathway in rBMSCs, similar to the results observed in vivo. Finally, BMS345541, an inhibitor of the NF‐κB signaling pathway, could reverse the effects of hyperoside on the biological functions in rBMSCs. In conclusion, our results suggest that hyperoside has potential therapeutic properties against periodontitis via promotion of proliferation and osteogenic differentiation of rBMSCs via activation of the NF‐κB signaling pathway. John Wiley and Sons Inc. 2020-08-18 /pmc/articles/PMC7459408/ /pubmed/32687664 http://dx.doi.org/10.1002/2211-5463.12937 Text en © 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Xu, Tao Wu, Xiao Zhou, Zhou Ye, Yu Yan, Chaoting Zhuge, Nanshan Yu, Jinhua Hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of BMSCs via activation of the NF‐κB pathway |
title | Hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of BMSCs via activation of the NF‐κB pathway |
title_full | Hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of BMSCs via activation of the NF‐κB pathway |
title_fullStr | Hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of BMSCs via activation of the NF‐κB pathway |
title_full_unstemmed | Hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of BMSCs via activation of the NF‐κB pathway |
title_short | Hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of BMSCs via activation of the NF‐κB pathway |
title_sort | hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of bmscs via activation of the nf‐κb pathway |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7459408/ https://www.ncbi.nlm.nih.gov/pubmed/32687664 http://dx.doi.org/10.1002/2211-5463.12937 |
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