Abstract
The objective was to compare the anti‐inflammatory potential of unprocessed and extruded amaranth pepsin/pancreatin hydrolysates in lipopolysaccharide (LPS)‐induced human THP‐1 and mouse RAW 264.7 macrophages. THP‐1 and RAW 264.7 cells were activated with LPS and treated with unprocessed and extruded amaranth hydrolysates (0.25 to 1.00 mg/mL). Peptides in extruded amaranth hydrolysates displayed antioxidant capacity, angiotensin converting enzyme‐inhibitor activity, antithrombotic and dipeptidyl peptidase‐IV inhibitor activity. Extruded amaranth (1 mg/mL) significantly reduced TNF‐α secretion in THP‐1 and RAW 264.7 cells by 36.5% and 33.5%, respectively; with concomitant reduction in PGE2 (15.4% and 31.4%, respectively), and reduction in COX‐2 (38.1% and 67.6%, respectively). Phosphorylation of IKK‐α was significantly reduced by 52.5% and 88.2% leading to reduced phosphorylation of IκB‐α (86.1% and 66.2%, respectively); resulting in reduction in the expression of p‐65 NF‐κB subunits in the nucleus by 64.2% for THP‐1 cells and 70.7% for RAW 264.7 cells. In conclusion, amaranth hydrolysates inhibited LPS‐induced inflammation in human and mouse macrophages by preventing activation of NF‐κB signaling. Extrusion improved the anti‐inflammatory effect of amaranth hydrolysates in both cell lines, which might be attributed to the production of bioactive peptides during processing.Grant Funding Source: University of Sinaloa Research Grant
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.