title: The anti-inflammatory effect of a glycosylation product derived from the high hydrostatic pressure enzymatic hydrolysate of a flatfish byproduct.
abstract: In this study, flatfish byproducts were hydrolyzed by Protamex at high hydrostatic pressure and glycosylated with ribose to utilize the protein of flatfish byproducts as a nutraceutical. We investigated the anti-inflammatory effects of glycosylated fish byproduct protein hydrolysate (GFPH) and its anti-inflammatory mechanisms were elucidated in lipopolysaccharide (LPS)-stimulated RAW 264.7 mouse macrophage. The results showed that GFPH suppresses LPS-induced production of nitric oxide (NO) and prostaglandin E2 (PGE2) and expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) dose-dependently. The enzyme-linked immunosorbent assay (ELISA) kit clearly demonstrated that GFPH significantly reduced the production of pro-inflammatory cytokines such as, interleukin (IL)-6, interleukin (IL)-1β and tumor necrosis factor (TNF)-α, and monocyte chemoattractant protein (MCP)-1. Moreover, GFPH reduced nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) activation. These results indicate that the inhibitory effects of GFPH on LPS-induced NO and PGE2 production might be due to the suppression of the NF-κB and MAPKs signaling pathways. Therefore, these results suggest that flatfish byproducts are latent bioactive resources and GFPH may have potential as a therapeutic agent in the treatment of various inflammatory diseases.
authors.affiliation: Department of Food Biotechnology, University of Science and Technology, Daejeon 305-350, South Korea.
authors.forename: In-Hu
authors.initials: IH
authors.lastname: Choe
authors.forename: Hyeon Jin
authors.initials: HJ
authors.lastname: Jeon
authors.forename: Sung-Hwan
authors.initials: SH
authors.lastname: Eom
authors.forename: Young-Ki
authors.initials: YK
authors.lastname: Han
authors.forename: Yoon Sook
authors.initials: YS
authors.lastname: Kim
authors.forename: Sang-Hoon
authors.initials: SH
authors.lastname: Lee
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D019587:Dietary Supplements; D015232:Dinoprostone / Q000378:metabolism; D005399:Fishes; D005511:Food Handling; D006031:Glycosylation; D006874:Hydrostatic Pressure; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D011492:Protein Hydrolysates / Q000494:pharmacology*; D000067996:RAW 264.7 Cells; D017747:Seafood / Q000032:analysis*; D015398:Signal Transduction
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D011492:Protein Hydrolysates; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D020928:Mitogen-Activated Protein Kinases; D015232:Dinoprostone