Abstract
SUMMARYNitric oxide (NO) plays a key role in the pathogenesis of inflammation and has been implicated in endotoxin-induced tissue injury. Chicken feather meal is a rich source of amino acids that may serve as a peptide hydrolysate to inhibit NO activity. Anti-inflammatory hydrolysates of chicken feather meal were prepared and fractionated into five samples based on molecular mass. The smallest fraction (<0.65 kDa) exhibited the highest NO inhibitory activity without cytotoxicity towards macrophage RAW 264.7 cells. Further subfractions were sufficient to obtain amino acid sequences by Q-TOF LC-MS/MS ESI analysis. Of these, the SNPSVAGVR (885.97 Da) peptide and its corresponding pure synthetic peptide have inhibitory activity against NO production by RAW 264.7 cells (IC50=(55.2±0.2) mM) without cytotoxicity. Reverse transcriptase polymerase chain reaction (RT-PCR) and quantitative real-time RT-PCR results revealed that the peptide of the obtained fraction reduced transcript expression levels of the pro-inflammatory cytokines iNOS, TNF-α, COX-2 and IL-6 in lipopolysaccharide-stimulated RAW 264.7 cells. These results suggest that the peptides derived from the chicken feather meal protein could potentially be used as a promising ingredient in functional foods or nutraceuticals against inflammatory diseases.
Highlights
Inflammation is a host defence mechanism that involves physiological and pathological processes within an organism, and is induced by the invasion of pathogens or tissue injury caused by biological, chemical or physical damage [1]
Proline, serine, glycine and leucine are present in higher mass fractions than other amino acids
Active anti-inflammatory peptides from Mytilus coruscus were reported to consist of glycine, valine, serine, leucine, glutamine and phenylalanine [5,27]
Summary
Inflammation is a host defence mechanism that involves physiological and pathological processes within an organism, and is induced by the invasion of pathogens or tissue injury caused by biological, chemical or physical damage [1]. The activation of several immune cells (monocytes and macrophages) produces inflammation mediators, such as nitric oxide (NO), cyclooxygenase-2 (COX-2), prostaglandins E2 (PGE2) and other pro-inflammatory cytokines (iNOS), including tumour necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β [2]. Inflammatory mediators, such as NO and PGE2, are produced via the oxidation of l-arginine by inducible nitric oxide synthase (iNOS) and the conversion of arachidonic acid by COX-2. Inflammation can be regulated by suppression of the pro-inflammatory cytokines and NO production [6]
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