Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 7, Issue 2, Pages 222-229Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2006.10.001
Keywords
eicosapentaenoic acid; microglia; NO; PGE2; proinflammatory cytokines; NF-kappa B; MAPKs; Akt
Categories
Ask authors/readers for more resources
Upon activation, microglia release proinflammatory mediators that play important roles in eliciting neuroinflammatory responses associated with neurodegenerative diseases. The anti-inflammatory properties of eicosapentaenoic acid (EPA) have been known, however, the effects responsible for lipopolysaccharide (LPS)-induced activation remain poorly understood in microglia. In the present study, we investigated the effects of EPA on the expression of proinflammatory mediators in LPS-stimulated BV2 microglia. EPA significantly inhibited the release of nitric oxide (NO), prostaglandin E-2 (PGE(2)) and proinflammatory cytokines such as interleukin (IL)-beta, IL-6 and tumor necrosis factor (TNF)-alpha in a dose-dependent manner. EPA also attenuated the production of cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) and proinflammatory cytokines at mRNA and/or protein levels. Moreover, EPA suppressed NF-KB activation by blocking IKB degradation, and also blocked the mitogen-activated protein kinases (MAPKs) such as ERK, p38 and JNK, and the Akt pathway. The anti-inflammatory properties of EPA may be useful for ameliorating neurodegenerative diseases as well as suppressing LPS-induced shock. (c) 2006 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available