A Novel Platelet Activating Factor Receptor Antagonist Reduces Cell Infiltration and Expression of Inflammatory Mediators in Mice Exposed to Desiccating Conditions after PRK

Purpose. To study the contribution of a novel PAF receptor antagonist LAU-0901 in the modulation of the increased inflammatory response in mice exposed to dessicating conditions (DE) after PRK. Methods. Eighty 13-14 week old female Balb/C mice were used. They were divided into two groups: One group...

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Main Authors: Salomon Esquenazi, Jiucheng He, Na Li, Nicolas G. Bazan, Isi Esquenazi, Haydee E. P. Bazan
Format: Article
Language:English
Published: Wiley 2009-01-01
Series:Clinical and Developmental Immunology
Online Access:http://dx.doi.org/10.1155/2009/138513
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author Salomon Esquenazi
Jiucheng He
Na Li
Nicolas G. Bazan
Isi Esquenazi
Haydee E. P. Bazan
author_facet Salomon Esquenazi
Jiucheng He
Na Li
Nicolas G. Bazan
Isi Esquenazi
Haydee E. P. Bazan
author_sort Salomon Esquenazi
collection DOAJ
description Purpose. To study the contribution of a novel PAF receptor antagonist LAU-0901 in the modulation of the increased inflammatory response in mice exposed to dessicating conditions (DE) after PRK. Methods. Eighty 13-14 week old female Balb/C mice were used. They were divided into two groups: One group was treated with LAU-0901 topical drops. The other group was treated with vehicle. In each group ten mice served as controls and ten were placed in DE. The other twenty mice underwent bilateral PRK and were divided in two additional groups: ten mice remained under normal conditions (NC) and the other ten were exposed to DE. After 1 week all animals underwent in vivo confocal microscopy, immunostaining and western blotting analysis. Results. Confocal microscopy showed an increased number of reflective structures in the corneal epithelium after PRK and exposure to DE in eyes treated with vehicle as compared to eyes treated with LAU-0901. Significant decrease of COX-2 and Arginase I expression and reduced alpha SMA cells was observed after PRK and exposure to DE in eyes treated with LAU-0901. Discussion: Exposure of mice to a DE after PRK increases the epithelial turnover rate. PAF is involved in the inflammatory cell infiltration and expression of inflammatory cytokines that follow PRK under DE.
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series Clinical and Developmental Immunology
spelling doaj-art-57c38e0a5b4641049974cec4d20129a92025-02-03T01:21:11ZengWileyClinical and Developmental Immunology1740-25221740-25302009-01-01200910.1155/2009/138513138513A Novel Platelet Activating Factor Receptor Antagonist Reduces Cell Infiltration and Expression of Inflammatory Mediators in Mice Exposed to Desiccating Conditions after PRKSalomon Esquenazi0Jiucheng He1Na Li2Nicolas G. Bazan3Isi Esquenazi4Haydee E. P. Bazan5LSU Eye Center and Neuroscience Center, LSU Health Sciences Center, School of Medicine, New Orleans, LA 70112, USALSU Eye Center and Neuroscience Center, LSU Health Sciences Center, School of Medicine, New Orleans, LA 70112, USALSU Eye Center and Neuroscience Center, LSU Health Sciences Center, School of Medicine, New Orleans, LA 70112, USALSU Eye Center and Neuroscience Center, LSU Health Sciences Center, School of Medicine, New Orleans, LA 70112, USALSU Eye Center and Neuroscience Center, LSU Health Sciences Center, School of Medicine, New Orleans, LA 70112, USALSU Eye Center and Neuroscience Center, LSU Health Sciences Center, School of Medicine, New Orleans, LA 70112, USAPurpose. To study the contribution of a novel PAF receptor antagonist LAU-0901 in the modulation of the increased inflammatory response in mice exposed to dessicating conditions (DE) after PRK. Methods. Eighty 13-14 week old female Balb/C mice were used. They were divided into two groups: One group was treated with LAU-0901 topical drops. The other group was treated with vehicle. In each group ten mice served as controls and ten were placed in DE. The other twenty mice underwent bilateral PRK and were divided in two additional groups: ten mice remained under normal conditions (NC) and the other ten were exposed to DE. After 1 week all animals underwent in vivo confocal microscopy, immunostaining and western blotting analysis. Results. Confocal microscopy showed an increased number of reflective structures in the corneal epithelium after PRK and exposure to DE in eyes treated with vehicle as compared to eyes treated with LAU-0901. Significant decrease of COX-2 and Arginase I expression and reduced alpha SMA cells was observed after PRK and exposure to DE in eyes treated with LAU-0901. Discussion: Exposure of mice to a DE after PRK increases the epithelial turnover rate. PAF is involved in the inflammatory cell infiltration and expression of inflammatory cytokines that follow PRK under DE.http://dx.doi.org/10.1155/2009/138513
spellingShingle Salomon Esquenazi
Jiucheng He
Na Li
Nicolas G. Bazan
Isi Esquenazi
Haydee E. P. Bazan
A Novel Platelet Activating Factor Receptor Antagonist Reduces Cell Infiltration and Expression of Inflammatory Mediators in Mice Exposed to Desiccating Conditions after PRK
Clinical and Developmental Immunology
title A Novel Platelet Activating Factor Receptor Antagonist Reduces Cell Infiltration and Expression of Inflammatory Mediators in Mice Exposed to Desiccating Conditions after PRK
title_full A Novel Platelet Activating Factor Receptor Antagonist Reduces Cell Infiltration and Expression of Inflammatory Mediators in Mice Exposed to Desiccating Conditions after PRK
title_fullStr A Novel Platelet Activating Factor Receptor Antagonist Reduces Cell Infiltration and Expression of Inflammatory Mediators in Mice Exposed to Desiccating Conditions after PRK
title_full_unstemmed A Novel Platelet Activating Factor Receptor Antagonist Reduces Cell Infiltration and Expression of Inflammatory Mediators in Mice Exposed to Desiccating Conditions after PRK
title_short A Novel Platelet Activating Factor Receptor Antagonist Reduces Cell Infiltration and Expression of Inflammatory Mediators in Mice Exposed to Desiccating Conditions after PRK
title_sort novel platelet activating factor receptor antagonist reduces cell infiltration and expression of inflammatory mediators in mice exposed to desiccating conditions after prk
url http://dx.doi.org/10.1155/2009/138513
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