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Sulforaphane protects against oxidative stress-induced apoptosis via activating SIRT1 in mouse osteoarthritis
Osteoarthritis (OA), the most common form of human joint disease, is characterized by progressive degeneration of the articular cartilage, synovitis and subchondral osteoporosis. Chondrocyte apoptosis is the primary pathogenic mechanism of OA and is considered to be a potential therapeutic target. S...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8258469/ https://www.ncbi.nlm.nih.gov/pubmed/34184072 http://dx.doi.org/10.3892/mmr.2021.12251 |
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author | Chen, Mangmang Huang, Lipeng Lv, Yangxun Li, Liubing Dong, Qirong |
author_facet | Chen, Mangmang Huang, Lipeng Lv, Yangxun Li, Liubing Dong, Qirong |
author_sort | Chen, Mangmang |
collection | PubMed |
description | Osteoarthritis (OA), the most common form of human joint disease, is characterized by progressive degeneration of the articular cartilage, synovitis and subchondral osteoporosis. Chondrocyte apoptosis is the primary pathogenic mechanism of OA and is considered to be a potential therapeutic target. Sulforaphane (SFN), a dietary isothiocyanate obtained from cruciferous vegetables, has been reported to exert an anti-apoptotic effect by activating sirtuin 1 (SIRT1). To the best of our knowledge, however, the effects of SFN on apoptotic responses in OA have not been reported. In the present study, SFN was shown to significantly inhibit chondrocyte apoptosis while enhancing expression levels of SIRT1 in a H(2)O(2)-induced OA mouse model. The anti-apoptotic effect of SFN was reversed by SIRT1 small interfering RNA, implying that SIRT1 exerted a protective role against the effect of SFN on chondrocytes. The expression levels of C/EBP homologous protein, 78-kDa glucose regulated protein, Bax, Bcl-2 and cleaved caspase 3 were found to be downregulated in SFN-treated mice. Furthermore, SFN ameliorated cartilage degradation in the OA mouse model. These findings indicate that SFN exerted an anti-apoptotic effect on chondrocytes and ameliorated OA in vivo by activating the SIRT1 signaling pathway. |
format | Online Article Text |
id | pubmed-8258469 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-82584692021-07-14 Sulforaphane protects against oxidative stress-induced apoptosis via activating SIRT1 in mouse osteoarthritis Chen, Mangmang Huang, Lipeng Lv, Yangxun Li, Liubing Dong, Qirong Mol Med Rep Articles Osteoarthritis (OA), the most common form of human joint disease, is characterized by progressive degeneration of the articular cartilage, synovitis and subchondral osteoporosis. Chondrocyte apoptosis is the primary pathogenic mechanism of OA and is considered to be a potential therapeutic target. Sulforaphane (SFN), a dietary isothiocyanate obtained from cruciferous vegetables, has been reported to exert an anti-apoptotic effect by activating sirtuin 1 (SIRT1). To the best of our knowledge, however, the effects of SFN on apoptotic responses in OA have not been reported. In the present study, SFN was shown to significantly inhibit chondrocyte apoptosis while enhancing expression levels of SIRT1 in a H(2)O(2)-induced OA mouse model. The anti-apoptotic effect of SFN was reversed by SIRT1 small interfering RNA, implying that SIRT1 exerted a protective role against the effect of SFN on chondrocytes. The expression levels of C/EBP homologous protein, 78-kDa glucose regulated protein, Bax, Bcl-2 and cleaved caspase 3 were found to be downregulated in SFN-treated mice. Furthermore, SFN ameliorated cartilage degradation in the OA mouse model. These findings indicate that SFN exerted an anti-apoptotic effect on chondrocytes and ameliorated OA in vivo by activating the SIRT1 signaling pathway. D.A. Spandidos 2021-08 2021-06-28 /pmc/articles/PMC8258469/ /pubmed/34184072 http://dx.doi.org/10.3892/mmr.2021.12251 Text en Copyright: © Chen et al. https://creativecommons.org/licenses/by-nc-nd/4.0/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 Chen, Mangmang Huang, Lipeng Lv, Yangxun Li, Liubing Dong, Qirong Sulforaphane protects against oxidative stress-induced apoptosis via activating SIRT1 in mouse osteoarthritis |
title | Sulforaphane protects against oxidative stress-induced apoptosis via activating SIRT1 in mouse osteoarthritis |
title_full | Sulforaphane protects against oxidative stress-induced apoptosis via activating SIRT1 in mouse osteoarthritis |
title_fullStr | Sulforaphane protects against oxidative stress-induced apoptosis via activating SIRT1 in mouse osteoarthritis |
title_full_unstemmed | Sulforaphane protects against oxidative stress-induced apoptosis via activating SIRT1 in mouse osteoarthritis |
title_short | Sulforaphane protects against oxidative stress-induced apoptosis via activating SIRT1 in mouse osteoarthritis |
title_sort | sulforaphane protects against oxidative stress-induced apoptosis via activating sirt1 in mouse osteoarthritis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8258469/ https://www.ncbi.nlm.nih.gov/pubmed/34184072 http://dx.doi.org/10.3892/mmr.2021.12251 |
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