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Inhibitory effects of eicosapentaenoic acid on lipopolysaccharide-induced activation in BV2 microglia
Dong-Oh Moon1, Ki-Cheon Kim, Cheng-Yun Jin
1Faculty of Applied Marine Science, Cheju National University, Jeju, South Korea.
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.
Insights
Eicosapentaenoic acid (EPA) reduces inflammation in microglia by inhibiting key signaling pathways. This suggests EPA could help treat neurodegenerative diseases and LPS-induced shock.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia activation releases mediators contributing to neuroinflammation in neurodegenerative diseases.
- Eicosapentaenoic acid (EPA) possesses known anti-inflammatory properties, but its effects on lipopolysaccharide (LPS)-induced microglial activation are not fully understood.
Purpose of the Study:
- To investigate the effects of EPA on the expression of pro-inflammatory mediators in LPS-stimulated BV2 microglia.
- To elucidate the molecular mechanisms underlying EPA's anti-inflammatory actions in microglia.
Main Methods:
- BV2 microglia were stimulated with LPS and treated with varying doses of EPA.
- Assessed the release of nitric oxide (NO) and prostaglandin E2 (PGE2).
- Measured mRNA and protein levels of pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha), COX-2, and iNOS.
- Investigated the impact of EPA on NF-kappaB, MAPK (ERK, p38, JNK), and Akt signaling pathways.
Main Results:
- EPA significantly inhibited the dose-dependent release of NO, PGE2, IL-1beta, IL-6, and TNF-alpha.
- EPA attenuated the production of COX-2, iNOS, and pro-inflammatory cytokines at both mRNA and protein levels.
- EPA suppressed NF-kappaB activation by inhibiting IkappaB degradation and blocked the ERK, p38, JNK, and Akt pathways.
Conclusions:
- EPA exhibits significant anti-inflammatory effects in LPS-stimulated microglia.
- EPA's mechanism involves the suppression of key inflammatory signaling pathways, including NF-kappaB and MAPKs.
- EPA holds potential therapeutic value for neurodegenerative diseases and LPS-induced shock.
