Ecklonia cava ethanolic extracts inhibit lipopolysaccharide-induced cyclooxygenase-2 and inducible nitric oxide synthase expression in BV2 microglia via the MAP kinase and NF-kappaB pathways.

Ecklonia cava (EC) is a brown alga that has demonstrated radical scavenging, bactericidal, tyrosinase inhibitory, and protease inhibitory activities. However, the molecular mechanisms underlying its anti-inflammatory action remain unclear. In the current study, we attempted to determine whether pretreatment with EC induces a significant inhibition of anti-inflammatory activity in lipopolysaccharide (LPS)-stimulated murine BV2 microglia. Our results indicate that EC inhibits LPS-induced nitric oxide (NO) and prostaglandin E(2) (PGE(2)) production in a concentration-dependent manner and inhibits inducible nitric oxide (iNOS) and cyclooxygenase (COX)-2 in BV2 microglia without significant cytotoxicity. EC treatment significantly reduced nuclear factor-kappaB (NF-kappaB) translocation and DNA-binding in LPS-stimulated BV2 microglia. This effect was mediated through the inhibition of the degradation of the inhibitor kappaB and by inhibition of the mitogen-activated protein kinase (MAPK) phosphorylation, at least in part by inhibiting the generation of reactive oxygen species. Our data also indicate that EC extracts exert anti-inflammatory effects by suppressing proinflammatory cytokines. Collectively, these results suggest that EC suppresses the induction of cytokines by LPS, as well as iNOS and COX-2 expression, by blocking NF-kappaB and MAPK activation. These findings provide mechanistic insights into the anti-inflammatory and neuroprotective actions of EC in BV2 microglia.