PMID- 24891839 OWN - NLM STAT- PubMed-not-MEDLINE DCOM- 20140603 LR - 20240321 IS - 1477-5956 (Print) IS - 1477-5956 (Electronic) IS - 1477-5956 (Linking) VI - 12 DP - 2014 TI - Pepsin-pancreatin protein hydrolysates from extruded amaranth inhibit markers of atherosclerosis in LPS-induced THP-1 macrophages-like human cells by reducing expression of proteins in LOX-1 signaling pathway. PG - 30 LID - 10.1186/1477-5956-12-30 [doi] AB - BACKGROUND: Atherosclerosis is considered a progressive disease that affects arteries that bring blood to the heart, to the brain and to the lower end. It derives from endothelial dysfunction and inflammation, which play an important role in the thrombotic complications of atherosclerosis. Cardiovascular disease is the leading cause of death around the world and one factor that can contribute to its progression and prevention is diet. Our previous study found that amaranth hydrolysates inhibited LPS-induced inflammation in human and mouse macrophages by preventing activation of NF-kappaB signaling. Furthermore, extrusion improved the anti-inflammatory effect of amaranth protein hydrolysates in both cell lines, probably attributed to the production of bioactive peptides during processing. Therefore, the objective of this study was to compare the anti-atherosclerotic potential of pepsin-pancreatin hydrolysates from unprocessed and extruded amaranth in THP-1 lipopolysaccharide-induced human macrophages and suggest the mechanism of action. RESULTS: Unprocessed amaranth hydrolysate (UAH) and extruded amaranth hydrolysate (EAH) showed a significant reduction in the expression of interleukin-4 (IL-4) (69% and 100%, respectively), interleukin-6 (IL-6) (64% and 52%, respectively), interleukin-22 (IL-22) (55% and 70%, respectively). Likewise, UAH and EAH showed a reduction in the expression of monocyte-chemo attractant protein-1 (MCP-1) (35% and 42%, respectively), transferrin receptor-1 (TfR-1) (48% and 61%, respectively), granulocyte-macrophage colony-stimulating factor (GM-CSF) (59% and 63%, respectively), and tumor necrosis factor-alpha (TNF-alpha) (60% and 63%, respectively). Also, EAH reduced the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) (27%), intracellular adhesion molecule-1 (ICAM-1) (28%) and matrix metalloproteinase-9 (MMP-9) (19%), important molecular markers in the atherosclerosis pathway. EAH, led to a reduction of 58, 52 and 79% for LOX-1, ICAM-1 and MMP-9, respectively, by confocal microscopy. CONCLUSIONS: Extruded amaranth hydrolysate showed potential anti-atherosclerotic effect in LPS-induced THP-1 human macrophage-like cells by reducing the expression of proteins associated with LOX-1 signaling pathway. FAU - Montoya-Rodriguez, Alvaro AU - Montoya-Rodriguez A AD - Programa Regional del Noroeste para el Doctorado en Biotecnologia, FCQB-UAS, Ciudad Universitaria, AP 1354, Culiacan, Sinaloa CP 80000, Mexico ; Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, 228 ERML, MC-051, 1201 West, Gregory Drive, Urbana, IL 61801, USA. FAU - Milan-Carrillo, Jorge AU - Milan-Carrillo J AD - Programa Regional del Noroeste para el Doctorado en Biotecnologia, FCQB-UAS, Ciudad Universitaria, AP 1354, Culiacan, Sinaloa CP 80000, Mexico. FAU - Dia, Vermont P AU - Dia VP AD - Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, 228 ERML, MC-051, 1201 West, Gregory Drive, Urbana, IL 61801, USA. FAU - Reyes-Moreno, Cuauhtemoc AU - Reyes-Moreno C AD - Programa Regional del Noroeste para el Doctorado en Biotecnologia, FCQB-UAS, Ciudad Universitaria, AP 1354, Culiacan, Sinaloa CP 80000, Mexico. FAU - Gonzalez de Mejia, Elvira AU - Gonzalez de Mejia E AD - Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, 228 ERML, MC-051, 1201 West, Gregory Drive, Urbana, IL 61801, USA. LA - eng PT - Journal Article DEP - 20140519 PL - England TA - Proteome Sci JT - Proteome science JID - 101170539 PMC - PMC4041052 OTO - NOTNLM OT - Amaranth OT - Atherosclerosis OT - Hydrolysates OT - Macrophages OT - THP-1 EDAT- 2014/06/04 06:00 MHDA- 2014/06/04 06:01 PMCR- 2014/05/19 CRDT- 2014/06/04 06:00 PHST- 2014/02/28 00:00 [received] PHST- 2014/05/08 00:00 [accepted] PHST- 2014/06/04 06:00 [entrez] PHST- 2014/06/04 06:00 [pubmed] PHST- 2014/06/04 06:01 [medline] PHST- 2014/05/19 00:00 [pmc-release] AID - 1477-5956-12-30 [pii] AID - 10.1186/1477-5956-12-30 [doi] PST - epublish SO - Proteome Sci. 2014 May 19;12:30. doi: 10.1186/1477-5956-12-30. eCollection 2014.