Anti-inflammatory action of high molecular weight Mytilus edulis hydrolysates fraction in LPS-induced RAW264.7 macrophage via NF-κB and MAPK pathways

• Published in: Food chemistry 2016-07, Vol.202, p.9-14
• Main Authors: Kim, Young-Sang, Ahn, Chang-Bum, Je, Jae-Young
• Format: Article
• Language: English
• Subjects: Animals; Anti-Inflammatory Agents - pharmacology; Anti-inflammatory effect; Cyclooxygenase 2 - genetics; Cyclooxygenase 2 - metabolism; Dinoprostone - antagonists & inhibitors; Dinoprostone - secretion; Gene Expression Regulation; I-kappa B Proteins - genetics; I-kappa B Proteins - metabolism; Interleukin-1beta - genetics; Interleukin-1beta - metabolism; Interleukin-6 - genetics; Interleukin-6 - metabolism; Lipopolysaccharides - toxicity; MAPKs; Mice; Molecular Weight; Mytilus edulis; Mytilus edulis - chemistry; NF-kappa B - genetics; NF-kappa B - metabolism; NF-KappaB Inhibitor alpha; NF-κB; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - genetics; Nitric Oxide Synthase Type II - metabolism; Phosphorylation; Protein hydrolysate; Protein Hydrolysates - chemistry; Protein Hydrolysates - pharmacology; RAW 264.7 Cells; RAW264.7 macrophages; Signal Transduction; Tumor Necrosis Factor-alpha - genetics; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 0308-8146; 1873-7072
• DOI: 10.1016/j.foodchem.2016.01.114

•Anti-inflammatory peptide fraction was generated from M. edulis by peptic hydrolysis.•High molecular weight peptide fraction (>5kDa) showed the best anti-inflammatory activity.•Anti-inflammatory action was attributed to the inhibition of NF-κB and MAPK signaling pathways. Anti-inflammatory Mytilus edulis hydrolysates (MEHs) were prepared by peptic hydrolysis and MEH was further fractionated into three fractions based on molecular weight, namely >5kDa, 1–5kDa, and 5kDa peptide fraction exerted the highest nitric oxide (NO) inhibitory activity and inhibited prostaglandin E2 (PGE2) secretion in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Pretreatment with the >5kDa peptide fraction markedly inhibited LPS-stimulated inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein and gene expressions. Stimulation by LPS induced the production of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and -1β (IL-1β), whereas co-treatment with the >5kDa peptide fraction suppressed pro-inflammatory cytokine production. The >5kDa peptide fraction inhibited the translocation of NF-κB (nuclear factor-kappa B) through the prevention of IκBα (inhibitory factor kappa B alpha) phosphorylation and degradation and also inhibited the MAPK signaling pathway in LPS-stimulated RAW264.7 macrophages.