Abstract
Objective: Investigate the effects of triamcinolone on transcript levels of the inflammatory markers (COX-2, TGF-β1, IL-1β) and tight junction proteins (zonula occludin-1 (ZO-1), occludin, E-cadherin, β-catenin) in an in vivo model of acute phonotrauma. We hypothesized that triamcinolone downregulates inflammatory mediator gene expression and upregulates tight junction gene expression.
Method: Eight New Zealand white rabbits received intralaryngeal triamcinolone acetonide at the following concentrations: saline control, 100 µg/25 µL, 400 µg/25 µL, and 800 µg/25 mL followed by 30 minutes of raised intensity phonation. Quantitative polymerase chain reaction (qPCR) was used to investigate gene expression levels of inflammatory markers and epithelial tight junction proteins.
Results: Results of qPCR revealed dose-dependent changes in COX-2, TGF-β1, and IL-1β. Higher concentrations of triamcinolone showed an inverse relationship with transcription of these gene products. For tight junction proteins, qPCR showed upregulated gene expression of ZO-1, occludin, and E-cadherin in rabbits receiving 100 µg/25 µL triamcinolone compared to controls. However, higher concentrations of triamcinolone resulted in decreased levels of tight junction gene expression.
Conclusion: Triamcinolone is used for treatment of laryngeal disorders. However, the anti-inflammatory properties of triamcinolone have not been demonstrated in the larynx. Results of this experiment provide support for the hypothesis that triamcinolone downregulates inflammatory mediator gene expression and upregulates tight junction gene expression at lower concentrations in acute phonotrauma.
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