Docosahexaenoic acid supplementation modifies fatty acid incorporation in tissues and prevents hypoxia induced-atherosclerosis progression in apolipoprotein-E deficient mice

Prostaglandins Leukot Essent Fatty Acids. 2014 Oct;91(4):111-7. doi: 10.1016/j.plefa.2014.07.016. Epub 2014 Aug 4.

Abstract

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.

Keywords: Atherosclerosis; Docosahexaenoic acid; Eicosapentaenoic acid; Inflammation; Intermittent hypoxia; Omega 3 polyunsaturated fatty acid.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apolipoproteins E / deficiency*
  • Apolipoproteins E / genetics
  • Atherosclerosis / drug therapy*
  • Atherosclerosis / metabolism*
  • Docosahexaenoic Acids / therapeutic use*
  • Fatty Acids / metabolism*
  • Hypoxia / physiopathology*
  • Male
  • Mice
  • Mice, Knockout

Substances

  • Apolipoproteins E
  • Fatty Acids
  • Docosahexaenoic Acids