A Polysaccharide Isolated from Ecklonia cava Fermented by Lactobacillus brevis Inhibits the Inflammatory Response by Suppressing the Activation of Nuclear Factor-κB in Lipopolysaccharide-Induced RAW 264.7 Macrophages

Abstract

We previously reported that the increment of carbohydrate content in the Viscozyme^® L (Novozyme Corp., Oklahoma City, OK, USA) extract of Lactobacillus brevis–fermented Ecklonia cava affected the inhibition of nitric oxide (NO) production and that it might be related to the polysaccharide compound. However, there is no report of anti-inflammatory effects of the polysaccharide or its biological mechanism. Here, we investigated the anti-inflammatory effects of the polysaccharide and its biological mechanism in lipopolysaccharide (LPS)-activated RAW 264.7 cells. The polysaccharide isolated from the Viscozyme extract of L. brevis–fermented E. cava (VLFEP) dose-dependently decreased LPS-stimulated NO production without cytotoxicity. Also, VLFEP significantly decreased the production of prostaglandin E₂ (PGE₂) at the 100 μg/mL concentration. In addition, VLFEP dose-dependently decreased the protein and mRNA expressions of inducible NO synthase, whereas it slightly decreased those of cyclooxygenase 2 and only at the 100 μg/mL concentration. Moreover, VLEFP dose-dependently decreased the productions and/or mRNA expressions of tumor necrosis factor-α and interleukin-6, compared with those of LPS only–stimulated cells. In further experiments, VLFEP considerably reduced the phosphorylation and degradation of inhibitory κB as well as the translocation of nuclear transcription factor-κB (NF-κB) p65 into the nucleus, and its DNA binding was markedly induced by LPS stimulation. This study suggests that VLFEP exerts anti-inflammatory effects by down-regulating the production and expression of pro-inflammatory cytokines and mediators via inhibiting the NF-κB pathway in LPS-stimulated RAW 264.7 cells.