Ciglitazone inhibits cigarette smoke solution-induced inflammatory responses in human middle ear epithelial cells

Hyung Jin Jun, Hyun Woo Lim, June Choi, Hak Hyun Jung, Sung Won Chae

Research output: Contribution to journalArticle

3 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)1136-1139
Number of pages4
JournalInternational Journal of Pediatric Otorhinolaryngology
Issue number8
Publication statusPublished - 2012 Aug


  • COX-2
  • Human middle ear epithelial cells
  • Otitis media
  • Peroxisome proliferator activated receptor gamma
  • Smoking
  • TNF-α

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Otorhinolaryngology

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