Arthropod steroid hormone (20-Hydroxyecdysone) suppresses IL-1β- induced catabolic gene expression in cartilage

Shiow Yunn Sheu; Shin Rong Ho; Jui Sheng Sun; Ching Yun Chen; Cherng Jyh Ke

doi:10.1186/s12906-015-0520-z

Arthropod steroid hormone (20-Hydroxyecdysone) suppresses IL-1β- induced catabolic gene expression in cartilage

Shiow Yunn Sheu, Shin Rong Ho, Jui Sheng Sun, Ching Yun Chen, Cherng Jyh Ke

Research output: Contribution to journal › Article › peer-review

19 Citations (Scopus)

Abstract

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^-8M 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.

Original language	English
Article number	1
Journal	BMC Complementary and Alternative Medicine
Volume	15
Issue number	1
DOIs	https://doi.org/10.1186/s12906-015-0520-z
Publication status	Published - Jan 24 2015

Keywords

20-Hydroxyecdysone
Cartilage destruction
HIF-2α
Hypoxia
IL-1β
Normoxia

ASJC Scopus subject areas

Complementary and alternative medicine

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10.1186/s12906-015-0520-z

Cite this

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title = "Arthropod steroid hormone (20-Hydroxyecdysone) suppresses IL-1β- induced catabolic gene expression in cartilage",

abstract = "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 10-8M 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.",

keywords = "20-Hydroxyecdysone, Cartilage destruction, HIF-2α, Hypoxia, IL-1β, Normoxia",

author = "Sheu, {Shiow Yunn} and Ho, {Shin Rong} and Sun, {Jui Sheng} and Chen, {Ching Yun} and Ke, {Cherng Jyh}",

note = "Funding Information: The authors wish to acknowledge The National Science Council, Taiwan, ROC and Research Fund of Taipei City Hospital, Taipei, Taiwan, ROC for their funding assistance for this work. We also thank the staff of the Second Core Lab, Department of Medical Research, National Taiwan University Hospital for technical support during the study. Publisher Copyright: {\textcopyright} 2015 Sheu et al.; licensee BioMed Central.",

year = "2015",

month = jan,

day = "24",

doi = "10.1186/s12906-015-0520-z",

language = "English",

volume = "15",

journal = "BMC Complementary and Alternative Medicine",

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T1 - Arthropod steroid hormone (20-Hydroxyecdysone) suppresses IL-1β- induced catabolic gene expression in cartilage

AU - Sheu, Shiow Yunn

AU - Ho, Shin Rong

AU - Sun, Jui Sheng

AU - Chen, Ching Yun

AU - Ke, Cherng Jyh

N1 - Funding Information: The authors wish to acknowledge The National Science Council, Taiwan, ROC and Research Fund of Taipei City Hospital, Taipei, Taiwan, ROC for their funding assistance for this work. We also thank the staff of the Second Core Lab, Department of Medical Research, National Taiwan University Hospital for technical support during the study. Publisher Copyright: © 2015 Sheu et al.; licensee BioMed Central.

PY - 2015/1/24

Y1 - 2015/1/24

N2 - 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 10-8M 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.

AB - 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 10-8M 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.

KW - 20-Hydroxyecdysone

KW - Cartilage destruction

KW - HIF-2α

KW - Hypoxia

KW - IL-1β

KW - Normoxia

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Arthropod steroid hormone (20-Hydroxyecdysone) suppresses IL-1β- induced catabolic gene expression in cartilage

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