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Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats
INTRODUCTION: Osteoarthritis (OA) is the most common disease, which seriously affects the daily life of the elderly. Currently, no traditional or drug therapy has been shown to explicitly block the progression of OA. Salidroside (Sal) is a bioactive component of Rhodiola rosea, which has many benefi...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7166061/ https://www.ncbi.nlm.nih.gov/pubmed/32341638 http://dx.doi.org/10.2147/DDDT.S242862 |
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author | Gao, Hui Peng, Lu Li, Chao Ji, Qinlong Li, Ping |
author_facet | Gao, Hui Peng, Lu Li, Chao Ji, Qinlong Li, Ping |
author_sort | Gao, Hui |
collection | PubMed |
description | INTRODUCTION: Osteoarthritis (OA) is the most common disease, which seriously affects the daily life of the elderly. Currently, no traditional or drug therapy has been shown to explicitly block the progression of OA. Salidroside (Sal) is a bioactive component of Rhodiola rosea, which has many beneficial effects on human health. However, the role and mechanism of Sal in OA have not been reported. METHODS: We established an anterior cruciate ligament transection (ACLT)-induced OA Rat model. The rats were divided into five groups (n = 10): Control group; ACLT group; ACLT + Sal (12.5 mg/kg) group; ACLT + Sal (25 mg/kg) group; ACLT + Sal (50 mg/kg) group. RESULTS: The study showed that Sal could significantly promote the proliferation of chondrocytes in OA rats induced by ACLT and restore the histological alteration of cartilage. Besides, Sal upregulated the levels of Collagen II and Aggrecan, and downregulated the level of MMP-13. Furthermore, Sal could reduce the number of CD4+IL-17(+) cells and decrease the levels of IL-17, IKBα and p65, while elevating the number of CD4+IL-10(+) cells and the level of IL-10. The decrease of IL-17 further inhibited the dissociation of IKBα to p65, thus reducing the release of TNF-α and VCAM-1. Taken together, Sal alleviates cartilage degeneration through promoting chondrocytes proliferation, inhibiting collagen fibrosis, and regulating inflammation and immune responses via NF-κB pathway in ACLT-induced OA Rats. DISCUSSION: Collectively, our study investigates the role and mechanism of Sal in OA, which lays a foundation for the application of Sal in OA. |
format | Online Article Text |
id | pubmed-7166061 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-71660612020-04-27 Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats Gao, Hui Peng, Lu Li, Chao Ji, Qinlong Li, Ping Drug Des Devel Ther Original Research INTRODUCTION: Osteoarthritis (OA) is the most common disease, which seriously affects the daily life of the elderly. Currently, no traditional or drug therapy has been shown to explicitly block the progression of OA. Salidroside (Sal) is a bioactive component of Rhodiola rosea, which has many beneficial effects on human health. However, the role and mechanism of Sal in OA have not been reported. METHODS: We established an anterior cruciate ligament transection (ACLT)-induced OA Rat model. The rats were divided into five groups (n = 10): Control group; ACLT group; ACLT + Sal (12.5 mg/kg) group; ACLT + Sal (25 mg/kg) group; ACLT + Sal (50 mg/kg) group. RESULTS: The study showed that Sal could significantly promote the proliferation of chondrocytes in OA rats induced by ACLT and restore the histological alteration of cartilage. Besides, Sal upregulated the levels of Collagen II and Aggrecan, and downregulated the level of MMP-13. Furthermore, Sal could reduce the number of CD4+IL-17(+) cells and decrease the levels of IL-17, IKBα and p65, while elevating the number of CD4+IL-10(+) cells and the level of IL-10. The decrease of IL-17 further inhibited the dissociation of IKBα to p65, thus reducing the release of TNF-α and VCAM-1. Taken together, Sal alleviates cartilage degeneration through promoting chondrocytes proliferation, inhibiting collagen fibrosis, and regulating inflammation and immune responses via NF-κB pathway in ACLT-induced OA Rats. DISCUSSION: Collectively, our study investigates the role and mechanism of Sal in OA, which lays a foundation for the application of Sal in OA. Dove 2020-04-14 /pmc/articles/PMC7166061/ /pubmed/32341638 http://dx.doi.org/10.2147/DDDT.S242862 Text en © 2020 Gao et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Gao, Hui Peng, Lu Li, Chao Ji, Qinlong Li, Ping Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats |
title | Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats |
title_full | Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats |
title_fullStr | Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats |
title_full_unstemmed | Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats |
title_short | Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats |
title_sort | salidroside alleviates cartilage degeneration through nf-κb pathway in osteoarthritis rats |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7166061/ https://www.ncbi.nlm.nih.gov/pubmed/32341638 http://dx.doi.org/10.2147/DDDT.S242862 |
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