Extrusion improved the anti-inflammatory effect of amaranth (Amaranthus hypochondriacus) hydrolysates in LPS-induced human THP-1 macrophage-like and mouse RAW 264.7 macrophages by preventing activation of NF-κB signaling.

METHODS

The objective was to compare the anti-inflammatory potential of unprocessed and extruded amaranth pepsin/pancreatin hydrolysates in LPS-induced human THP-1 macrophages-like and mouse RAW 264.7 macrophages focusing on their anti-inflammatory mechanism of action related to NF-κB signaling pathway.

RESULTS

Amaranth hydrolysates were characterized by MS-MS and tested for anti-inflammatory effects on human and mouse macrophages. Peptides found in extruded amaranth hydrolysates displayed antioxidant capacity, angiotensin converting enzyme-inhibitor activity, and dipeptidyl peptidase-IV inhibitor activity. Gly-Pro-Arg peptide was present and reported as antithrombotic. Extruded amaranth hydrolysates (1 mg/mL) significantly reduced tumor necrosis factor alpha 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%), and 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 a reduction in the expression of p65 NF-κB subunits in the nucleus by 64.2% for THP-1 and 70.7% for RAW 264.7 cells.

CONCLUSIONS

Amaranth hydrolysates inhibited LPS-induced inflammation in human and mouse macrophages by preventing activation of NF-κB signaling. Extrusion improved anti-inflammatory effect of amaranth hydrolysates in both cells, which might be attributed to the production of bioactive peptides during processing.