Anti-inflammatory action of high molecular weight Mytilus edulis hydrolysates fraction in LPS-induced RAW264.7 macrophage via NF-κB and MAPK pathways. (1st July 2016)

• Record Type: Journal Article
• Authors: Kim, Young-Sang; Ahn, Chang-Bum; Je, Jae-Young
• Is Part Of: Food chemistry. Volume 202(2016)
• Page Start: 9
• Page End: 14
• Publication Date: 2016-07-01
• Subjects: Mytilus edulis -- Anti-inflammatory effect -- Protein hydrolysate -- NF-κB -- MAPKs -- RAW264.7 macrophages; Food -- Analysis -- Periodicals; Food -- Composition -- Periodicals; 664
• DOI: 10.1016/j.foodchem.2016.01.114
• Languages: English
• ISSNs: 0308-8146

Abstract

Highlights: Anti-inflammatory peptide fraction was generated from M. edulis by peptic hydrolysis. High molecular weight peptide fraction (>5 kDa) showed the best anti-inflammatory activity. Anti-inflammatory action was attributed to the inhibition of NF-κB and MAPK signaling pathways. Abstract: Anti-inflammatory Mytilus edulis hydrolysates (MEHs) were prepared by peptic hydrolysis and MEH was further fractionated into three fractions based on molecular weight, namely >5 kDa, 1–5 kDa, and <1 kDa. The >5 kDa 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 >5 kDa 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 >5 kDa peptide fraction suppressed pro-inflammatory cytokine production. The >5 kDa 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.