Anti-inflammatory effects of fucoidan through inhibition of NF-κB, MAPK and Akt activation in lipopolysaccharide-induced BV2 microglia cells

Fucoidan, a sulfated polysaccharide extracted from brown seaweed, displays a wide variety of internal biological activities; however, the cellular and molecular mechanisms underlying fucoidan's anti-inflammatory activity remain poorly understood. In this study, we investigated the inhibitory effects of fucoidan on production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators in BV2 microglia. Our data indicated that fucoidan treatment significantly inhibited excessive production of nitric oxide (NO) and prostaglandin E-2 (PGE(2)) in LPS-stimulated BV2 microglia. It also attenuated expression of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, monocyte chemoattractant protein-1 (MCP-1), and pro-inflammatory cytokines, including interleukin-1 beta (IL-1 beta) and tumor necrosis factor (TNF)-alpha. Moreover, fucoidan exhibited anti-inflammatory properties by suppression of nuclear factor-kappa B (NF-kappa B) activation and down-regulation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and AKT pathways. These finding suggest that fucoidan may offer substantial therapeutic potential for treatment of neurodegenerative diseases that are accompanied by microglial activation. (C) 2011 Elsevier Ltd. All rights reserved.