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Inhibitory effects of eicosapentaenoic acid on lipopolysaccharide-induced activation in BV2 microglia.

Abstract：

: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)-1beta, 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-kappaB activation by blocking IkappaB 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.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Moon DO,Kim KC,Jin CY,Han MH,Park C,Lee KJ,Park YM,Choi YH,Kim GY

doi

10.1016/j.intimp.2006.10.001

subject

Has Abstract

pub_date

2007-02-01 00:00:00

pages

222-9

issue

2

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(06)00306-7

journal_volume

7

pub_type

杂志文章

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