Document Detail

Caffeic acid phenethyl ester inhibits diesel exhaust particle-induced inflammation of human middle ear epithelial cells via NOX4 inhibition.
MedLine Citation:
PMID:  24224404     Owner:  NLM     Status:  In-Process    
OBJECTIVES: Otitis media is one of the most common diseases in pediatric populations. Recent research on its pathogenesis has focused on air pollution. Chronic exposure to particulate air pollution is associated with the impairment of middle ear function. However, the mechanisms and the underlying inhibitory pathways, especially in the human middle ear, remain unknown. Caffeic acid phenethyl ester (CAPE) is a biologically active ingredient of propolis, a product of honeybee hives, which has anti-oxidative and anti-inflammatory activities. The aim of this study was to evaluate the inhibitory effect of CAPE on diesel exhaust particle (DEP)-induced inflammation of human middle ear epithelial cells and to determine the underlying pathway of the action of CAPE.
METHODS: The inflammatory damage caused by DEPs and the anti-inflammatory effects of CAPE were determined by measuring the levels of tumor necrosis factor alpha and nicotinamide adenine dinucleotide phosphate oxidase (NOX) 4 with real-time reverse transcription polymerase chain reaction and Western blot analysis. The oxidative stress induced by DEPs and the anti-oxidative effects of CAPE were directly evaluated by measuring reactive oxygen species production by use of flow cytometric analysis of 2',7'-dichlorofluorescein diacetate. The effects of CAPE were compared with those of N-acetyl-L-cysteine, which has anti-oxidative and anti-inflammatory effects.
RESULTS: Use of CAPE significantly inhibited DEP-induced up-regulation of tumor necrosis factor alpha and NOX4 expression in a dose- and time-dependent manner. The accumulation of reactive oxygen species induced by DEPs was decreased by pretreatment with CAPE. The anti-inflammatory and anti-oxidative effects of CAPE were similar to those of N-acetyl-L-cysteine.
CONCLUSIONS: The inflammation induced by DEP is reduced by CAPE via the inhibition of NOX4 expression. These findings suggest that CAPE might be used as a therapeutic agent against DEP-induced inflammation of human middle ear epithelial cells.
Sun-Young Jo; Naree Lee; Sung-Moon Hong; Hak Hyun Jung; Sung-Won Chae
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Annals of otology, rhinology, and laryngology     Volume:  122     ISSN:  0003-4894     ISO Abbreviation:  Ann. Otol. Rhinol. Laryngol.     Publication Date:  2013 Sep 
Date Detail:
Created Date:  2013-11-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0407300     Medline TA:  Ann Otol Rhinol Laryngol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  595-600     Citation Subset:  AIM; IM    
Division of Brain Korea 21 Program for Biomedical Science, Korea University College of Medicine, Seoul, Korea.
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