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

2006; Elsevier BV; Volume: 7; Issue: 2 Linguagem: Inglês

10.1016/j.intimp.2006.10.001

1878-1705

Dong‐Oh Moon, Ki-Cheon Kim, Cheng‐Yun Jin, Min‐Ho Han, Cheol Park, Kyeong‐Jun Lee, Yeong‐Min Park, Yung Hyun Choi, Gi‐Young Kim,

NF-κB Signaling Pathways

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 E2 (PGE2) and proinflammatory cytokines such as interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α 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-κB activation by blocking IκB 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.