Peer-reviewed veterinary case report
Tepoxalin reduces cartilage breakdown in dog joint cells in lab test
By Macrory, Lisa et al.·Published in BMC veterinary research·2009·Faculty of Veterinary Science, United Kingdom·View original on PubMed →
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Original publication title: An exploration of the ability of tepoxalin to ameliorate the degradation of articular cartilage in a canine in vitro model.
- Species:
- dog
Plain-English summary
A study looked at how well tepoxalin, a medication that helps reduce inflammation, could protect cartilage in dogs with osteoarthritis. Researchers tested cartilage samples from seven healthy dogs and found that when they added inflammatory substances, the cartilage started to break down. However, when they treated the samples with tepoxalin, they noticed a decrease in collagen loss, suggesting that the drug could help slow down cartilage damage. While it didn't affect another type of cartilage component, the results indicate that tepoxalin may be beneficial for dogs suffering from joint issues.
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Abstract
BACKGROUND: To study the ability of tepoxalin, a dual inhibitor of cyclooxygenase (COX) and lipoxygenase (LOX) and its active metabolite to reduce the catabolic response of cartilage to cytokine stimulation in an in vitro model of canine osteoarthritis (OA).Grossly normal cartilage was collected post-mortem from seven dogs that had no evidence of joint disease. Cartilage explants were cultured in media containing the recombinant canine interleukin-1beta (IL-1beta) at 100 ng/ml and recombinant human oncostatin-M (OSM) at 50 ng/ml. The effects of tepoxalin and its metabolite were studied at three concentrations (1 x 10(-5), 1 x 10(-6) and 1 x 10(-7) M). Total glycosaminoglycan (GAG) and collagen (hydroxyproline) release from cartilage explants were used as outcome measures of proteoglycan and collagen depletion respectively. PGE2 and LTB4 assays were performed to study the effects of the drug on COX and LOX activity. RESULTS: Treatment with IL-1beta and OSM significantly upregulated both collagen (p = 0.004) and proteoglycan (p = 0.001) release from the explants. Tepoxalin at 10(-5) M and 10(-6) M caused a decrease in collagen release from the explants (p = 0.047 and p = 0.075). Drug treatment showed no effect on GAG release. PGE2 concentration in culture media at day 7 was significantly increased by IL-1beta and OSM and treatment with both tepoxalin and its metabolite showed a trend towards dose-dependent reduction of PGE2 production. LTB4 concentrations were too low to be quantified. Cytotoxicity assays suggested that neither tepoxalin nor its metabolite had a toxic effect on the cartilage chondrocytes at the concentrations and used in this study. CONCLUSION: This study provides evidence that tepoxalin exerts inhibition of COX and can reduce in vitro collagen loss from canine cartilage explants at a concentration of 10(-5) M. We can conclude that, in this model, tepoxalin can partially inhibit the development of cartilage degeneration when it is available locally to the tissue.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/19624842/