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    Please use this identifier to cite or link to this item: https://ir.lib.ncu.edu.tw/handle/987654321/102693


    Title: Arthropod steroid hormone (20-Hydroxyecdysone) suppresses IL-1β- induced catabolic gene expression in cartilage
    Authors: 陳靖昀;Sheu, Shiow-Yunn;Ho, Shin-Rong;Sun, Jui-Sheng;Chen, Ching-Yun;Ke, Cherng-Jyh
    Contributors: 生醫理工學院生醫科學與工程學系
    Keywords: Animals;Arthropoda;Arthropods;Basic Helix-Loop-Helix Transcription Factors - metabolism;Basic research;cartilage;Cartilage - drug effects;Cartilage - metabolism;Cartilage, Articular - drug effects;Cartilage, Articular - metabolism;catabolism;Cells, Cultured;Chiropractic Medicine;chondrocytes;Chondrocytes - drug effects;Chondrocytes - metabolism;collagen;Collagen Type II - metabolism;complement;Complementary & Alternative Medicine;Cytokines - metabolism;Down-Regulation;ecdysterone;Ecdysterone - pharmacology;Gene Expression;interleukin-1beta;Interleukin-1beta - metabolism;Internal Medicine;Male;Matrix Metalloproteinase 13 - genetics;Matrix Metalloproteinase 13 - metabolism;Matrix Metalloproteinase 3 - genetics;Matrix Metalloproteinase 3 - metabolism;Medicine;Medicine & Public Health;metalloproteinases;mice;Mice, Inbred ICR;neonates;osteoarthritis;Osteoarthritis - metabolism;Osteoarthritis - prevention & control;Research Article;steroid hormones;Synovial Membrane - metabolism;toxicity testing;transcription factors;Transcription Factors - metabolism;viability
    Date: 2015-01-24
    Issue Date: 2026-04-23 11:15:03 (UTC+8)
    Publisher: BioMed Central Ltd.;London: BioMed Central
    Abstract: 摘要: Background In osteoarthritis (OA), the imbalance of chondrocytes’ anabolic and catabolic factors can induce cartilage destruction. Interleukin-1 beta (IL-1β) is a potent pro-inflammatory cytokine that is capable of inducing chondrocytes and synovial cells to synthesize MMPs. The hypoxia-inducible factor-2alpha (HIF-2alpha, encoded by Epas1) is the catabolic transcription factor in the osteoarthritic process. The purpose of this study is to validate the effects of ecdysteroids (Ecd) on IL-1β- induced cartilage catabolism and the possible role of Ecd in treatment or prevention of early OA. Methods Chondrocytes and articular cartilage was harvested from newborn ICR mice. Ecd effect on chondrocytes viability was tested and the optimal concentration was determined by MTT assay. The effect of HIF-2α (EPAS1) in cartilage catabolism simulated by IL-1β (5 ng/ml) was evaluated by articular cartilage explants culture. The effects of Ecd on IL-1β-induced inflammatory conditions and their related catabolic genes expression were analyzed. Results Interleukin-1β (IL-1β) treatment on primary mouse articular cartilage explants enhanced their Epas1, matrix metalloproteinases (MMP-3, MMP-13) and ADAMTS-5 genes expression and down-regulated collagen type II (Col2a1) gene expression. With the pre-treatment of 10 −8 M Ecd, the catabolic effects of IL-1β on articular cartilage were scavenged. Conclusion In conclusions, Ecd can reduce the IL-1β-induced inflammatory effect of the cartilage. Ecd may suppress IL-1β- induced cartilage catabolism via HIF-2α pathway.
    其他題名: BMC Complement Altern Med
    出版者: London: BioMed Central
    出版日期: 2015-01-24
    出處: BMC complementary and alternative medicine, 2015-01, Vol.15 (1), p.1-1, Article 1
    資源來源: PubMed Central Open Access
    版權: Sheu et al.; licensee BioMed Central. 2015 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated.
    版權: Sheu et al.; licensee BioMed Central. 2015
    識別號: ISSN: 1472-6882
    識別號: EISSN: 1472-6882
    識別號: DOI: 10.1186/s12906-015-0520-z
    識別號: PMID: 25617057
    Appears in Collections:[Department of Biomedical Sciences and Engineering ] journal & Dissertation

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