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Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-κB p65 phosphorylation
The proliferation, migration and differentiation capacities of human periodontal ligament fibroblasts (HPDLCs) are important for the treatment of periodontal diseases. The aim of the present study was to investigate whether icariin could promote these abilities in HPDLCs, and explore the cellular me...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6102717/ https://www.ncbi.nlm.nih.gov/pubmed/30066868 http://dx.doi.org/10.3892/mmr.2018.9302 |
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author | Liu, Hai-Jiang Liu, Xue-Yang Jing, De-Bao |
author_facet | Liu, Hai-Jiang Liu, Xue-Yang Jing, De-Bao |
author_sort | Liu, Hai-Jiang |
collection | PubMed |
description | The proliferation, migration and differentiation capacities of human periodontal ligament fibroblasts (HPDLCs) are important for the treatment of periodontal diseases. The aim of the present study was to investigate whether icariin could promote these abilities in HPDLCs, and explore the cellular mechanisms therein. The results indicated that icarrin markedly blocked apoptosis, and increased the viability and migration of HPDLCs, particularly at the concentrations of 20 and 50 µM. In addition, icariin significantly promoted HPDLCs to synthesize extracellular matrix, which was reflected by the decreased expression of matrix matalloproteinase-1 and increased expression of tissue inhibitor of metalloproteinase-1. Furthermore, the levels of bone morphogenetic protein 2, collagen I, osteoprotegerin and alkaline phosphatase were markedly elevated by icariin, indicating that icariin was able to promote the osteogenic differentiation capability of HPDLCs. Icariin also inactivated the Toll-like receptor 4 (TLR)-4/nuclear factor (NF)-κB signaling pathway by suppressing the expression levels of TLR-4 and phosphorylated p65, and by blocking p65 nuclear translocation. These results suggested that icarrin increased the survival, migration and osteoblastic differentiation of HPDLCs by inhibiting the TLR-4/NF-κB signaling pathway. |
format | Online Article Text |
id | pubmed-6102717 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-61027172018-08-23 Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-κB p65 phosphorylation Liu, Hai-Jiang Liu, Xue-Yang Jing, De-Bao Mol Med Rep Articles The proliferation, migration and differentiation capacities of human periodontal ligament fibroblasts (HPDLCs) are important for the treatment of periodontal diseases. The aim of the present study was to investigate whether icariin could promote these abilities in HPDLCs, and explore the cellular mechanisms therein. The results indicated that icarrin markedly blocked apoptosis, and increased the viability and migration of HPDLCs, particularly at the concentrations of 20 and 50 µM. In addition, icariin significantly promoted HPDLCs to synthesize extracellular matrix, which was reflected by the decreased expression of matrix matalloproteinase-1 and increased expression of tissue inhibitor of metalloproteinase-1. Furthermore, the levels of bone morphogenetic protein 2, collagen I, osteoprotegerin and alkaline phosphatase were markedly elevated by icariin, indicating that icariin was able to promote the osteogenic differentiation capability of HPDLCs. Icariin also inactivated the Toll-like receptor 4 (TLR)-4/nuclear factor (NF)-κB signaling pathway by suppressing the expression levels of TLR-4 and phosphorylated p65, and by blocking p65 nuclear translocation. These results suggested that icarrin increased the survival, migration and osteoblastic differentiation of HPDLCs by inhibiting the TLR-4/NF-κB signaling pathway. D.A. Spandidos 2018-09 2018-07-23 /pmc/articles/PMC6102717/ /pubmed/30066868 http://dx.doi.org/10.3892/mmr.2018.9302 Text en Copyright: © Liu 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 Liu, Hai-Jiang Liu, Xue-Yang Jing, De-Bao Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-κB p65 phosphorylation |
title | Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-κB p65 phosphorylation |
title_full | Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-κB p65 phosphorylation |
title_fullStr | Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-κB p65 phosphorylation |
title_full_unstemmed | Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-κB p65 phosphorylation |
title_short | Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-κB p65 phosphorylation |
title_sort | icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting toll-like receptor 4 and nf-κb p65 phosphorylation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6102717/ https://www.ncbi.nlm.nih.gov/pubmed/30066868 http://dx.doi.org/10.3892/mmr.2018.9302 |
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