Effect of eicosapentaenoic acid-derived prostaglandin E3 on intestinal epithelial barrier function

被引：23
作者：
Rodriguez-Lagunas, Maria J. [1 ]
Ferrer, Ruth [1 ]
Moreno, Juan J. [1 ]
机构：
[1] Univ Barcelona, Fac Farm, Dept Fisiol, E-08028 Barcelona, Spain
来源：
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS | 2013年 / 88卷 / 05期
关键词：
Paracellular permeability; PGE(3); Inflammatory bowel disease; Caco-2; cells; TIGHT JUNCTION PERMEABILITY; POLYUNSATURATED FATTY-ACIDS; CACO-2 CELL MONOLAYERS; PARACELLULAR PERMEABILITY; MECHANISMS; RECEPTOR; MODULATION; EXPRESSION; INCREASE; DISEASE;
D O I：
10.1016/j.plefa.2013.02.001
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Prostaglandins (PG) are inflammatory mediators derived from arachidonic or eicosapentaenoic acid giving rise to the 2-series or the 3-series prostanoids, respectively. Previously, we have observed that PGE(2) disrupts epithelial barrier function. Considering the beneficial effect of fish oil consumption in intestinal inflammatory processes, the aim of this study was to assess the role of PGE(3) on epithelial barrier function assessed from transepithelial electrical resistance and dextran fluxes in Caco-2 cells. The results indicate that PGE(3) increased paracellular permeability (PP) to the same extent as PGE(2), through the interaction with EP1 and EP4 receptors and with intracellular Ca2+ and cAMP as the downstream targets. Moreover, we observed a redistribution of tight junction proteins, occludin and claudin-4. In conclusion, PGE(3) is able to increase PP thus leading to reconsider the role of PGE(2)/PGE(3) ratio in the beneficial effects of dietary fish oil supplementation in the disruption of barrier function. (c) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码：339 / 345
页数：7
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