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Effects of stanozolol on normal and IL-1β-stimulated equine chondrocytes in vitro

BACKGROUND: Intra-articular administration of stanozolol has shown promising results by improving the clinical management of lameness associated with naturally-occurring osteoarthritis (OA) in horses, and by decreasing osteophyte formation and subchondral bone reaction in sheep following surgically...

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Autores principales: Castro Martins, Mariana, Peffers, Mandy J., Lee, Katie, Rubio-Martinez, Luis M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5859414/
https://www.ncbi.nlm.nih.gov/pubmed/29554899
http://dx.doi.org/10.1186/s12917-018-1426-z
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author Castro Martins, Mariana
Peffers, Mandy J.
Lee, Katie
Rubio-Martinez, Luis M.
author_facet Castro Martins, Mariana
Peffers, Mandy J.
Lee, Katie
Rubio-Martinez, Luis M.
author_sort Castro Martins, Mariana
collection PubMed
description BACKGROUND: Intra-articular administration of stanozolol has shown promising results by improving the clinical management of lameness associated with naturally-occurring osteoarthritis (OA) in horses, and by decreasing osteophyte formation and subchondral bone reaction in sheep following surgically induced OA. However, there is limited evidence on the anti-inflammatory and modulatory properties of stanozolol on articular tissues. The objective of the current study was to evaluate the effects of stanozolol on chondrocyte viability and gene expression in normal equine chondrocytes and an inflammatory in vitro system of OA (interleukin-1β (IL-1β) treated chondrocytes). RESULTS: Chondrocytes from normal metacarpophalangeal joints of skeletally mature horses were exposed to four treatment groups: (1) media only (2) media+IL-1β (3) media+IL-1β + stanozolol (4) media+stanozolol. Following exposure, chondrocyte viability and the expression of catabolic, anabolic and structural genes were determined. General linear models with Dunnet’s comparisons with Bonferroni’s adjustment were performed. Cell viability was similar in all groups. Stanozolol treatment reduced gene expression of MMP-13, MMP-1, IL-6 and COX-2 in both normal and IL-1β treated chondrocytes. Stanozolol treatment reduced ADAMTS4 gene expression in normal chondrocytes. Stanozolol reduced the expression of COL2A1. CONCLUSIONS: The current study demonstrates stanozolol has chondroprotective effects through downregulation of genes for pro-inflammatory/catabolic cytokines and enzymes associated with OA. However, there is no evidence of increased cartilage stimulation through upregulation of the anabolic and structural genes tested.
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spelling pubmed-58594142018-03-20 Effects of stanozolol on normal and IL-1β-stimulated equine chondrocytes in vitro Castro Martins, Mariana Peffers, Mandy J. Lee, Katie Rubio-Martinez, Luis M. BMC Vet Res Research Article BACKGROUND: Intra-articular administration of stanozolol has shown promising results by improving the clinical management of lameness associated with naturally-occurring osteoarthritis (OA) in horses, and by decreasing osteophyte formation and subchondral bone reaction in sheep following surgically induced OA. However, there is limited evidence on the anti-inflammatory and modulatory properties of stanozolol on articular tissues. The objective of the current study was to evaluate the effects of stanozolol on chondrocyte viability and gene expression in normal equine chondrocytes and an inflammatory in vitro system of OA (interleukin-1β (IL-1β) treated chondrocytes). RESULTS: Chondrocytes from normal metacarpophalangeal joints of skeletally mature horses were exposed to four treatment groups: (1) media only (2) media+IL-1β (3) media+IL-1β + stanozolol (4) media+stanozolol. Following exposure, chondrocyte viability and the expression of catabolic, anabolic and structural genes were determined. General linear models with Dunnet’s comparisons with Bonferroni’s adjustment were performed. Cell viability was similar in all groups. Stanozolol treatment reduced gene expression of MMP-13, MMP-1, IL-6 and COX-2 in both normal and IL-1β treated chondrocytes. Stanozolol treatment reduced ADAMTS4 gene expression in normal chondrocytes. Stanozolol reduced the expression of COL2A1. CONCLUSIONS: The current study demonstrates stanozolol has chondroprotective effects through downregulation of genes for pro-inflammatory/catabolic cytokines and enzymes associated with OA. However, there is no evidence of increased cartilage stimulation through upregulation of the anabolic and structural genes tested. BioMed Central 2018-03-20 /pmc/articles/PMC5859414/ /pubmed/29554899 http://dx.doi.org/10.1186/s12917-018-1426-z Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Castro Martins, Mariana
Peffers, Mandy J.
Lee, Katie
Rubio-Martinez, Luis M.
Effects of stanozolol on normal and IL-1β-stimulated equine chondrocytes in vitro
title Effects of stanozolol on normal and IL-1β-stimulated equine chondrocytes in vitro
title_full Effects of stanozolol on normal and IL-1β-stimulated equine chondrocytes in vitro
title_fullStr Effects of stanozolol on normal and IL-1β-stimulated equine chondrocytes in vitro
title_full_unstemmed Effects of stanozolol on normal and IL-1β-stimulated equine chondrocytes in vitro
title_short Effects of stanozolol on normal and IL-1β-stimulated equine chondrocytes in vitro
title_sort effects of stanozolol on normal and il-1β-stimulated equine chondrocytes in vitro
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5859414/
https://www.ncbi.nlm.nih.gov/pubmed/29554899
http://dx.doi.org/10.1186/s12917-018-1426-z
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