Enzymatically Decomposed Antarctic Krill Oil Inhibits Atherosclerosis by Suppressing the Vascular Endothelial Inflammation
Antarctic krill (Euphausia superba) oil has emerged as a potential alternative for omega-3 supplementation and been shown to reduce cardiovascular disease risk. However, all relevant current krill oil extraction methods generally use organic solvents which could leave solvent residues on the final p...
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Published in | Food Supplements and Biomaterials for Health Vol. 1; no. 1; pp. 1 - 15 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
건강기능식품미래포럼
01.03.2021
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Subjects | |
Online Access | Get full text |
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Summary: | Antarctic krill (Euphausia superba) oil has emerged as a potential alternative for omega-3 supplementation and been shown to reduce cardiovascular disease risk. However, all relevant current krill oil extraction methods generally use organic solvents which could leave solvent residues on the final product. Hence, we established a solvent-free method by using proteases, evaluated effects of the enzymatically decomposed krill oil (EDKO) on vascular endothelial inflammation and atherosclerotic plaque formation, and explore its underlying mechanism of action. For these purposes, we prepared vascular inflammation model by partial carotid ligation in C57BL/6 mice and acute and chronic atherosclerosis models in apolipoprotein E knockout (ApoE−/−) mice, and examined the effects of EDKO on inflammatory gene expression in arterial endothelium and development of atherosclerosis, respectively. Our results showed administration of EDKO by oral gavage down-regulated the expressions of pro-inflammatory genes (vascular cell adhesion protein 1, intercellular adhesion molecule 1, chitinase 3 like 1, and chemokine [C-C motif ] ligand 19) in arterial endothelium and inhibited atherosclerotic plaque formation in both acute and chronic model. Our findings suggest that dietary supplementation of EDKO provides antiatherogenic benefits by inhibiting vascular inflammation through regulating inflammatory gene expressions in arterial endothelium. KCI Citation Count: 0 |
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Bibliography: | https://doi.org/10.52361/fsbh.2021.1.e9 |
ISSN: | 2765-4362 2765-4699 |
DOI: | 10.52361/fsbh.2021.1.e9 |