Objective: Peroxisome proliferator activated receptor-γ (PPAR-γ), a member of the nuclear hormone receptor superfamily, plays an important role in the regulation of mucosal inflammation. The aim of this study was to investigate the anti-inflammatory effect of a PPAR-γ agonist, ciglitazone, on cigarette smoke solution (CSS)-induced inflammation in human middle ear epithelial cell lines (HMEECs). Design: HMEECs with or without ciglitazone pre-treatment were exposed to CSS in order to induce the inflammatory response. The suppressive effect of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2(COX-2), were evaluated using real-time polymerase chain reaction and Western blotting. Results: Stimulation with CSS at 40. μg/ml for 6. h resulted in a 4.1-fold increase in the expression of TNF-α mRNA in the HMEECs. CSS-induced up-regulation of TNF-α mRNA was decreased by more than 2.8-fold in cells pre-treated with ciglitazone. The up-regulation of COX-2 mRNA and increased COX-2 protein expression induced by CSS were also inhibited by more than 3.7-fold with ciglitazone pre-treatment. Conclusions: These findings suggest that the inflammatory response induced by CSS could be inhibited by ciglitazone, a PPAR-γ agonist, in HMEECs. As such, PPAR-γ agonists may have therapeutic potential for the treatment of otitis media.
|Number of pages||4|
|Journal||International Journal of Pediatric Otorhinolaryngology|
|Publication status||Published - 2012 Aug|
Copyright 2013 Elsevier B.V., All rights reserved.
- Human middle ear epithelial cells
- Otitis media
- Peroxisome proliferator activated receptor gamma
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health