TY - JOUR
T1 - Ciglitazone inhibits cigarette smoke solution-induced inflammatory responses in human middle ear epithelial cells
AU - Jun, Hyung Jin
AU - Lim, Hyun Woo
AU - Choi, June
AU - Jung, Hak Hyun
AU - Chae, Sung Won
N1 - Copyright:
Copyright 2013 Elsevier B.V., All rights reserved.
PY - 2012/8
Y1 - 2012/8
N2 - 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.
AB - 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.
KW - COX-2
KW - Human middle ear epithelial cells
KW - Otitis media
KW - Peroxisome proliferator activated receptor gamma
KW - Smoking
KW - TNF-α
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U2 - 10.1016/j.ijporl.2012.04.017
DO - 10.1016/j.ijporl.2012.04.017
M3 - Article
C2 - 22609261
AN - SCOPUS:84862762616
SN - 0165-5876
VL - 76
SP - 1136
EP - 1139
JO - International Journal of Pediatric Otorhinolaryngology
JF - International Journal of Pediatric Otorhinolaryngology
IS - 8
ER -