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Perilla Oil Reduces Fatty Streak Formation at Aortic Sinus via Attenuation of Plasma Lipids and Regulation of Nitric Oxide Synthase in ApoE KO Mice
Author(s) -
Hong Sun Hee,
Kim Mijeong,
Noh Jeong Sook,
Song Yeong Ok
Publication year - 2016
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-016-4188-z
Subject(s) - fatty streak , medicine , nitric oxide synthase , endocrinology , chemistry , polyunsaturated fatty acid , nitric oxide , apolipoprotein e , enos , cholesterol , biochemistry , fatty acid , biology , disease
Consumption of n‐3 polyunsaturated fatty acids (PUFA) is associated with a reduced incidence of atherosclerosis. Perilla oil (PO) is a vegetable oil rich in α‐linolenic acid (ALA), an n‐3 PUFA. In this study, antiatherogenic effects and related mechanisms of PO were investigated in atherosclerotic mice. Apolipoprotein E knockout (ApoE KO) mice (male, n = 27) were fed high‐cholesterol and high‐fat diets containing 10 % w/w lard (LD), PO, or sunflower oil (SO) for 10 weeks. Plasma triglyceride, total cholesterol, and low‐density lipoprotein cholesterol concentrations reduced in the PO and SO groups compared to the concentrations in the LD group ( P < 0.05). The PO group showed reduced fatty streak lesion size at the aortic sinus ( P < 0.05) compared to the sizes in the LD and SO groups. A morphometric analysis showed enhancement of endothelial nitric oxide synthase expression and reduction of inducible nitric oxide synthase expression in the PO group compared to that in the LD group ( P < 0.05). Furthermore, aortic protein expression of intercellular cell adhesion molecule 1 and vascular cell adhesion molecule 1 was diminished in the PO group compared to that in the LD and SO groups ( P < 0.05). These findings suggested that PO inhibited the development of aortic atherosclerosis by improving the plasma lipid profile, regulating nitric oxide synthase, and suppressing the vascular inflammatory response in the aorta of ApoE KO mice.