interleukin-8 and 11-12-epoxy-5-8-14-eicosatrienoic-acid

interleukin-8 has been researched along with 11-12-epoxy-5-8-14-eicosatrienoic-acid* in 1 studies

Other Studies

1 other study(ies) available for interleukin-8 and 11-12-epoxy-5-8-14-eicosatrienoic-acid

Article	Year
Epoxyeicosatrienoic acids attenuate cigarette smoke extract-induced interleukin-8 production in bronchial epithelial cells. Prostaglandins, leukotrienes, and essential fatty acids, 2015, Volume: 94 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. Topics: 8,11,14-Eicosatrienoic Acid; Anti-Inflammatory Agents; Bronchi; Cell Line; Cytochrome P-450 CYP2J2; Cytochrome P-450 Enzyme System; Epithelial Cells; Gene Expression Regulation; Humans; Interleukin-8; MAP Kinase Signaling System; Smoking; Vasodilator Agents	2015

Article

Year

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

Prostaglandins, leukotrienes, and essential fatty acids, 2015, Volume: 94

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.

Topics: 8,11,14-Eicosatrienoic Acid; Anti-Inflammatory Agents; Bronchi; Cell Line; Cytochrome P-450 CYP2J2; Cytochrome P-450 Enzyme System; Epithelial Cells; Gene Expression Regulation; Humans; Interleukin-8; MAP Kinase Signaling System; Smoking; Vasodilator Agents

2015