NDLI: Epoxyeicosatrienoic acids attenuate cigarette smoke extract-induced interleukin-8 production in bronchial epithelial cells.

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Epoxyeicosatrienoic acids attenuate cigarette smoke extract-induced interleukin-8 production in bronchial epithelial cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ma, Wen-Jiang Sun, Yan-Hong Jiang, Jun-Xia Dong, Xin-Wei Zhou, Jian-Ying Xie, Qiang-Min
Description	Country affiliation: China Author Affiliation: Ma WJ ( The First Affiliated Hospital of Medical College, Zhejiang University, Hangzhou 310009, China.); Sun YH ( Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Medical College of Zhejiang University, Hangzhou 310058, China.); Jiang JX ( Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Medical College of Zhejiang University, Hangzhou 310058, China.); Dong XW ( Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Medical College of Zhejiang University, Hangzhou 310058, China.); Zhou JY ( The First Affiliated Hospital of Medical College, Zhejiang University, Hangzhou 310009, China. Electronic address: Drzjy@163.com.); Xie QM ( Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Medical College of Zhejiang University, Hangzhou 310058, China)
Abstract	In response to endothelial cell activation, arachidonic acid can be converted by cytochrome P450 (CYP) epoxygenases to epoxyeicosatrienoic acids (EETs), which have potent vasodilator and anti-inflammatory properties. In this study, we investigated the effects of exogenous EETs on cigarette smoke extract (CSE)-induced inflammation in human bronchial epithelial cells (NCI-H292). We found that CSE inhibited the expression of CYP2C8 and mildly stimulated the expression of epoxide hydrolase 2 (EPHX2) but did not change the expression of CYP2J2. Treatment with 11,12-EET or 14,15-EET attenuated the CSE-induced release of interleukin (IL)-8 by inhibiting the phosphorylation of p38 mitogen-activated protein kinases (MAPKs). Our results demonstrated that CSE may reduce the anti-inflammatory ability of epithelial cells themselves by lowering the EET level. EETs from pulmonary epithelial cells may play a critical protective role on epithelial cell injury.
File Format	HTM / HTML
ISSN	09523278
Volume Number	94
e-ISSN	15322823
Journal	Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA)
Language	English
Publisher	Elsevier
Publisher Date	2015-03-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Endocrinology 8,11,14-eicosatrienoic Acid Pharmacology Anti-inflammatory Agents Bronchi Cytology Epithelial Cells Drug Effects Interleukin-8 Genetics Smoking Adverse Effects Analogs & Derivatives Cell Line Cytochrome P-450 Enzyme System Metabolism Gene Expression Regulation Humans Map Kinase Signaling System Vasodilator Agents Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Clinical Biochemistry

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