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Resveratrol rescues TNF-α-induced inhibition of osteogenesis in human periodontal ligament stem cells via the ERK1/2 pathway
Periodontitis is a common inflammatory disorder affecting the tissues surrounding the teeth, which can lead to the destruction of periodontal tissue and tooth loss. Resveratrol, a natural phytoalexin, exerts multiple biological effects. For example, its anti-inflammatory activity has been widely stu...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7115248/ https://www.ncbi.nlm.nih.gov/pubmed/32186753 http://dx.doi.org/10.3892/mmr.2020.11021 |
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author | Yuan, Jiakan Wang, Xuxia Ma, Dan Gao, Hui Zheng, Dehua Zhang, Jun |
author_facet | Yuan, Jiakan Wang, Xuxia Ma, Dan Gao, Hui Zheng, Dehua Zhang, Jun |
author_sort | Yuan, Jiakan |
collection | PubMed |
description | Periodontitis is a common inflammatory disorder affecting the tissues surrounding the teeth, which can lead to the destruction of periodontal tissue and tooth loss. Resveratrol, a natural phytoalexin, exerts multiple biological effects. For example, its anti-inflammatory activity has been widely studied for the treatment of inflammatory bowel disease for a number of years. However, its effect on bone repair and new bone formation in an inflammatory microenvironment is not well understood. Accordingly, the effect of resveratrol on inflammation-affected human periodontal ligament stem cells (hPDLSCs) requires further investigation. In the present study, the effect of tumor necrosis factor-α (TNF-α), resveratrol, or the combination of both on the osteogenic differentiation of hPDLSCs, as well as the underlying mechanisms involved, were investigated. Cell Counting Kit-8 assay, alkaline phosphatase staining, Alizarin red staining, Oil Red O staining, reverse transcription-quantitative PCR and western blotting were used in the present study. It was demonstrated that resveratrol enhanced hPDLSC osteogenesis and reversed the inhibitory effects of TNF-α on this process. Further mechanistic studies indicated that resveratrol exerted anti-inflammatory activity by activating the ERK1/2 pathway, decreasing the secretion of interleukin (IL)-6 and IL-8 induced by TNF-α, and enhancing hPDLSCs osteogenesis. The present study suggested that resveratrol may be a novel and promising therapeutic choice for periodontitis. |
format | Online Article Text |
id | pubmed-7115248 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-71152482020-04-08 Resveratrol rescues TNF-α-induced inhibition of osteogenesis in human periodontal ligament stem cells via the ERK1/2 pathway Yuan, Jiakan Wang, Xuxia Ma, Dan Gao, Hui Zheng, Dehua Zhang, Jun Mol Med Rep Articles Periodontitis is a common inflammatory disorder affecting the tissues surrounding the teeth, which can lead to the destruction of periodontal tissue and tooth loss. Resveratrol, a natural phytoalexin, exerts multiple biological effects. For example, its anti-inflammatory activity has been widely studied for the treatment of inflammatory bowel disease for a number of years. However, its effect on bone repair and new bone formation in an inflammatory microenvironment is not well understood. Accordingly, the effect of resveratrol on inflammation-affected human periodontal ligament stem cells (hPDLSCs) requires further investigation. In the present study, the effect of tumor necrosis factor-α (TNF-α), resveratrol, or the combination of both on the osteogenic differentiation of hPDLSCs, as well as the underlying mechanisms involved, were investigated. Cell Counting Kit-8 assay, alkaline phosphatase staining, Alizarin red staining, Oil Red O staining, reverse transcription-quantitative PCR and western blotting were used in the present study. It was demonstrated that resveratrol enhanced hPDLSC osteogenesis and reversed the inhibitory effects of TNF-α on this process. Further mechanistic studies indicated that resveratrol exerted anti-inflammatory activity by activating the ERK1/2 pathway, decreasing the secretion of interleukin (IL)-6 and IL-8 induced by TNF-α, and enhancing hPDLSCs osteogenesis. The present study suggested that resveratrol may be a novel and promising therapeutic choice for periodontitis. D.A. Spandidos 2020-05 2020-03-11 /pmc/articles/PMC7115248/ /pubmed/32186753 http://dx.doi.org/10.3892/mmr.2020.11021 Text en Copyright: © Yuan et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Yuan, Jiakan Wang, Xuxia Ma, Dan Gao, Hui Zheng, Dehua Zhang, Jun Resveratrol rescues TNF-α-induced inhibition of osteogenesis in human periodontal ligament stem cells via the ERK1/2 pathway |
title | Resveratrol rescues TNF-α-induced inhibition of osteogenesis in human periodontal ligament stem cells via the ERK1/2 pathway |
title_full | Resveratrol rescues TNF-α-induced inhibition of osteogenesis in human periodontal ligament stem cells via the ERK1/2 pathway |
title_fullStr | Resveratrol rescues TNF-α-induced inhibition of osteogenesis in human periodontal ligament stem cells via the ERK1/2 pathway |
title_full_unstemmed | Resveratrol rescues TNF-α-induced inhibition of osteogenesis in human periodontal ligament stem cells via the ERK1/2 pathway |
title_short | Resveratrol rescues TNF-α-induced inhibition of osteogenesis in human periodontal ligament stem cells via the ERK1/2 pathway |
title_sort | resveratrol rescues tnf-α-induced inhibition of osteogenesis in human periodontal ligament stem cells via the erk1/2 pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7115248/ https://www.ncbi.nlm.nih.gov/pubmed/32186753 http://dx.doi.org/10.3892/mmr.2020.11021 |
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