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Endogenously decreasing tissue n-6/n-3 fatty acid ratio reduces atherosclerotic lesions in apolipoprotein E-deficient mice by inhibiting systemic and vascular inflammation
Wan J.-B.1; Huang L.-L.1; Rong R.1; Tan R.1; Wang J.1; Kang J.X.1
2010-12-01
Source PublicationArteriosclerosis, Thrombosis, and Vascular Biology
ISSN10795642
Volume30Issue:12Pages:2487-2494
Abstract

Objective- To use the fat-1 transgenic mouse model to determine the role of tissue n-6/n-3 fatty acid ratio in atherosclerotic plaque formation. Although it has been suggested that a low ratio of n-6/n-3 polyunsaturated fatty acids (PUFAs) is more desirable in reducing the risk of atherosclerotic cardiovascular disease, the role of tissue n-6/n-3 fatty acid ratio in atherosclerosis has not been sufficiently tested in a well-controlled experimental system. The fat-1 transgenic mouse model, expressing an n-3 fatty acid desaturase, is capable of producing n-3 PUFAs from n-6 PUFAs and thereby has a ratio of n-6/n-3 fatty acids close to 1:1 in tissues and organs. Methods and Results- To generate apolipoprotein E-deficient plus fat-1 transgenic mice (apoE/fat-1), we crossed heterozygous fat-1 mice with apoE mice. After 14 weeks of a Western-type diet rich in n-6 PUFAs, the apoE/fat-1 mice showed a lower ratio of n-6/n-3 fatty acids than the apoE mice in all organs and tissues tested. The aortic lesion area in apoE/fat-1 mice was significantly reduced when compared with that of apoE littermates (7.14±0.54% versus 13.49±1.61%). There were no differences in plasma cholesterol or high- and low-density lipoprotein levels between the 2 groups, except for a higher triglyceride level in the apoE/fat-1 mice. A significant reduction of interleukin 6 and prostaglandin E2 in both plasma and aorta culture medium was observed in apoE/fat-1 mice. RT-PCR analysis also indicated that the expression of intercellular adhesion molecule-1, monocyte chemoattractant protein-1, interleukin 6, and cyclooxygenase-2 was lower in the aortas and the circulating monocytes from apoE/fat-1 mice. In addition, the expression of nuclear factor κB/p65 in the aorta and the recruitment of macrophages into atherosclerotic plaques were reduced in apoE/fat-1 mice, compared with apoE mice. Conclusion- To our knowledge, this is the first study to provide direct evidence for the role of tissue n-6/n-3 ratio in atherosclerosis using the fat-1 transgenic mouse model. Our findings demonstrate that a decreased n-6/n-3 fatty acid ratio reduces atherosclerotic lesions in apoE mice. This protective effect may be attributed to the antiinflammatory properties of n-3 fatty acids, rather than their lipid-lowering effect. © 2010 American Heart Association. All rights reserved.

KeywordAtherosclerosis Fat-1 Transgenic Mice Inflammation N-3 Fatty Acids N-6/n-3 Fatty Acid Ratio
DOI10.1161/ATVBAHA.110.210054
URLView the original
Indexed BySCI
WOS Research AreaHematology ; Cardiovascular System & Cardiology
WOS SubjectHematology ; Peripheral Vascular Disease
WOS IDWOS:000284309000034
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Cited Times [WOS]:64   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Affiliation1.Massachusetts General Hospital
2.Sun Yat-Sen University
Recommended Citation
GB/T 7714
Wan J.-B.,Huang L.-L.,Rong R.,et al. Endogenously decreasing tissue n-6/n-3 fatty acid ratio reduces atherosclerotic lesions in apolipoprotein E-deficient mice by inhibiting systemic and vascular inflammation[J]. Arteriosclerosis, Thrombosis, and Vascular Biology,2010,30(12):2487-2494.
APA Wan J.-B.,Huang L.-L.,Rong R.,Tan R.,Wang J.,&Kang J.X..(2010).Endogenously decreasing tissue n-6/n-3 fatty acid ratio reduces atherosclerotic lesions in apolipoprotein E-deficient mice by inhibiting systemic and vascular inflammation.Arteriosclerosis, Thrombosis, and Vascular Biology,30(12),2487-2494.
MLA Wan J.-B.,et al."Endogenously decreasing tissue n-6/n-3 fatty acid ratio reduces atherosclerotic lesions in apolipoprotein E-deficient mice by inhibiting systemic and vascular inflammation".Arteriosclerosis, Thrombosis, and Vascular Biology 30.12(2010):2487-2494.
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