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Psoralen promotes the expression of cyclin D1 in chondrocytes via the Wnt/β-catenin signaling pathway
Psoralen (PSO), the active ingredient of Fructus Psoraleae (FP) the dried ripe fruit of Psoralea corylifolia L., has been commonly used in traditional Chinese medicine (TCM) for the treatment of osteoarthritis (OA). We found that PSO activates cartilaginous cellular functions of rat chondrocytes in...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5627873/ https://www.ncbi.nlm.nih.gov/pubmed/28949389 http://dx.doi.org/10.3892/ijmm.2017.3148 |
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author | Zheng, Wenwei Lin, Pingdong Ma, Yuhuan Shao, Xiang Chen, Houhuang Chen, Da Liu, Xianxiang Li, Xihai Ye, Hongzhi |
author_facet | Zheng, Wenwei Lin, Pingdong Ma, Yuhuan Shao, Xiang Chen, Houhuang Chen, Da Liu, Xianxiang Li, Xihai Ye, Hongzhi |
author_sort | Zheng, Wenwei |
collection | PubMed |
description | Psoralen (PSO), the active ingredient of Fructus Psoraleae (FP) the dried ripe fruit of Psoralea corylifolia L., has been commonly used in traditional Chinese medicine (TCM) for the treatment of osteoarthritis (OA). We found that PSO activates cartilaginous cellular functions of rat chondrocytes in vitro. However, the effect of PSO on chondrocyte proliferation and the precise mechanisms involved remain to be elucidated. We investigated the effects of PSO on chondrocytes isolated from Sprague-Dawley (SD) rats and evaluated involvement of the Wnt/β-catenin signaling pathway. The viability of chondrocytes treated with PSO was increased in a dose- and time-dependent manner, as assessed by MTT assay. We found that the gene expression and protein levels of Wnt-4, Frizzled-2, β-catenin and cyclin D1 in the PSO-treated chondrocytes were significantly upregulated, while the gene expression and protein level of glycogen synthase kinase-3β (GSK-3β) were downregulated, compared with the untreated chondrocytes. By immunofluorescence, we also found that PSO induced β-catenin nuclear translocation. Importantly, the expression of β-catenin and cyclin D1 was partly inhibited by Dickkopf-1 (DKK-1), an inhibitor of the Wnt/β-catenin signaling pathway. Additionally, Col-II expression in chondrocytes was increased after treatment with PSO. Taken together, these results indicate that PSO promotes chondrocyte proliferation by activating the Wnt/β-catenin signaling pathway, and it may play an important role in the treatment of OA. |
format | Online Article Text |
id | pubmed-5627873 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-56278732017-10-08 Psoralen promotes the expression of cyclin D1 in chondrocytes via the Wnt/β-catenin signaling pathway Zheng, Wenwei Lin, Pingdong Ma, Yuhuan Shao, Xiang Chen, Houhuang Chen, Da Liu, Xianxiang Li, Xihai Ye, Hongzhi Int J Mol Med Articles Psoralen (PSO), the active ingredient of Fructus Psoraleae (FP) the dried ripe fruit of Psoralea corylifolia L., has been commonly used in traditional Chinese medicine (TCM) for the treatment of osteoarthritis (OA). We found that PSO activates cartilaginous cellular functions of rat chondrocytes in vitro. However, the effect of PSO on chondrocyte proliferation and the precise mechanisms involved remain to be elucidated. We investigated the effects of PSO on chondrocytes isolated from Sprague-Dawley (SD) rats and evaluated involvement of the Wnt/β-catenin signaling pathway. The viability of chondrocytes treated with PSO was increased in a dose- and time-dependent manner, as assessed by MTT assay. We found that the gene expression and protein levels of Wnt-4, Frizzled-2, β-catenin and cyclin D1 in the PSO-treated chondrocytes were significantly upregulated, while the gene expression and protein level of glycogen synthase kinase-3β (GSK-3β) were downregulated, compared with the untreated chondrocytes. By immunofluorescence, we also found that PSO induced β-catenin nuclear translocation. Importantly, the expression of β-catenin and cyclin D1 was partly inhibited by Dickkopf-1 (DKK-1), an inhibitor of the Wnt/β-catenin signaling pathway. Additionally, Col-II expression in chondrocytes was increased after treatment with PSO. Taken together, these results indicate that PSO promotes chondrocyte proliferation by activating the Wnt/β-catenin signaling pathway, and it may play an important role in the treatment of OA. D.A. Spandidos 2017-11 2017-09-21 /pmc/articles/PMC5627873/ /pubmed/28949389 http://dx.doi.org/10.3892/ijmm.2017.3148 Text en Copyright: © Zheng 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 Zheng, Wenwei Lin, Pingdong Ma, Yuhuan Shao, Xiang Chen, Houhuang Chen, Da Liu, Xianxiang Li, Xihai Ye, Hongzhi Psoralen promotes the expression of cyclin D1 in chondrocytes via the Wnt/β-catenin signaling pathway |
title | Psoralen promotes the expression of cyclin D1 in chondrocytes via the Wnt/β-catenin signaling pathway |
title_full | Psoralen promotes the expression of cyclin D1 in chondrocytes via the Wnt/β-catenin signaling pathway |
title_fullStr | Psoralen promotes the expression of cyclin D1 in chondrocytes via the Wnt/β-catenin signaling pathway |
title_full_unstemmed | Psoralen promotes the expression of cyclin D1 in chondrocytes via the Wnt/β-catenin signaling pathway |
title_short | Psoralen promotes the expression of cyclin D1 in chondrocytes via the Wnt/β-catenin signaling pathway |
title_sort | psoralen promotes the expression of cyclin d1 in chondrocytes via the wnt/β-catenin signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5627873/ https://www.ncbi.nlm.nih.gov/pubmed/28949389 http://dx.doi.org/10.3892/ijmm.2017.3148 |
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