Caffeic acid phenethyl ester inhibits diesel exhaust particle-induced inflammation of human middle ear epithelial cells via NOX4 inhibition

Sun Young Jo, Naree Lee, Sung Moon Hong, Hak Hyun Jung, Sungwon Chae

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

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 a 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 a 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. All rights reserved

Original languageEnglish
Pages (from-to)595-600
Number of pages6
JournalAnnals of Otology, Rhinology and Laryngology
Volume122
Issue number9
DOIs
Publication statusPublished - 2013 Jan 1

Fingerprint

Vehicle Emissions
Otitis Media
Epithelial Cells
Anti-Inflammatory Agents
Air Pollution
Acetylcysteine
Middle Ear
Reactive Oxygen Species
caffeic acid phenethyl ester
Tumor Necrosis Factor-alpha
Propolis
Urticaria
NADP
Reverse Transcription
Oxidoreductases
Oxidative Stress
Up-Regulation
Western Blotting

Keywords

  • Diesel
  • Nicotinamide adenine dinucleotide phosphate oxidase
  • Otitis media

ASJC Scopus subject areas

  • Otorhinolaryngology

Cite this

Caffeic acid phenethyl ester inhibits diesel exhaust particle-induced inflammation of human middle ear epithelial cells via NOX4 inhibition. / Jo, Sun Young; Lee, Naree; Hong, Sung Moon; Jung, Hak Hyun; Chae, Sungwon.

In: Annals of Otology, Rhinology and Laryngology, Vol. 122, No. 9, 01.01.2013, p. 595-600.

Research output: Contribution to journalArticle

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abstract = "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 a 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 a 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. All rights reserved",
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