Docosahexaenoic acid supplementation modifies fatty acid incorporation in tissues and prevents hypoxia induced-atherosclerosis progression in apolipoprotein-E deficient mice
Autor: | Laetitia Van Noolen, Amandine Rey, Magnus Bäck, Patrice Faure, Claire Arnaud, Patrick Levy, Françoise Stanke-Labesque, Marcelo H. Petri |
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Rok vydání: | 2014 |
Předmět: |
Apolipoprotein E
Male medicine.medical_specialty Apolipoprotein B Docosahexaenoic Acids Clinical Biochemistry Biology chemistry.chemical_compound Mice Apolipoproteins E Internal medicine medicine Animals Hypoxia chemistry.chemical_classification Mice Knockout Fatty Acids food and beverages Fatty acid Intermittent hypoxia Cell Biology Atherosclerosis Eicosapentaenoic acid Endocrinology chemistry Docosahexaenoic acid biology.protein lipids (amino acids peptides and proteins) Arachidonic acid Polyunsaturated fatty acid |
Zdroj: | Prostaglandins, leukotrienes, and essential fatty acids. 91(4) |
ISSN: | 1532-2823 |
Popis: | The n -3 polyunsaturated fatty acid, docosahexaenoic acid (DHA), displays anti-inflammatory properties that may prevent atherosclerosis progression. Exposure of apolipoprotein-E deficient (ApoE −/− ) mice to chronic intermittent hypoxia (CIH) accelerates atherosclerosis progression. Our aim was to assess DHA-supplementation influence on fatty acid incorporation in different tissues/organs and on atherosclerosis progression in ApoE −/− mice exposed to CIH. ApoE −/− mice were exposed to CIH or normoxia (N) and randomized to four groups (N control, CIH control, N+DHA, and CIH+DHA). DHA-supplementation enhanced DHA and reduced arachidonic acid (AA) contents in tissues/organs. CIH control mice exhibited increased atherosclerosis lesion sizes compared to N control mice. DHA prevented CIH induced atherosclerosis but did not improve atherosclerosis burden in N mice. Aortic matrix metalloproteinase-2 (MMP-2) expression was decreased in CIH+DHA mice ( p =0.007). DHA-supplementation prevented CIH-induced atherosclerosis acceleration. This was associated with a decrease of AA incorporation and of aortic MMP-2 gene expression. |
Databáze: | OpenAIRE |
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