title: Long-term effects of resveratrol supplementation on suppression of atherogenic lesion formation and cholesterol synthesis in apo E-deficient mice.
abstract: Atherosclerosis is a chronic inflammatory disease of the arteries resulting from interactions between lipids, monocytes, and arterial wall cells. The effects of resveratrol supplements (RV, 0.02% and 0.06% each, w/w) with regard to the modulation of lipid profiles, cholesterol synthesis, and anti-atherogenesis were examined in apo E-deficient (apo E(-/-)) mice fed a normal diet. The concentration of total-cholesterol (total-C) and LDL-cholesterol (LDL-C) in plasma was significantly lower in the resveratrol-supplemented groups compare to the control group over the entire experimental period. The plasma HDL-C concentration was significantly elevated, and the ratio of HDL-C/total-C was significantly higher in the CF and RV groups than in the control group. Plasma paraoxonase (PON) activity was significantly higher in the 0.06% resveratrol group. The hepatic HMG-CoA reductase (HMGR) activity was significantly lower in the clofibrate and resveratrol groups than in the control group. Resveratrol supplements attenuated the presence of atherosclerotic lesions and periarterial fat deposition in the apo E(-/-) mice. The presence of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in atherosclerotic vessels was diminished in the resveratrol-supplemented apo E(-/-) mice. These results provide new insight into the anti-atherogenic and hypocholesterolemic properties of resveratrol in apo E(-/-) mice that were fed a normal diet.
authors.affiliation: Department of Food Science and Nutrition, Kyungpook National University, 1370, Sankyuk-Dong, Buk-Gu, Daegu, Republic of Korea.
authors.forename: Gyeong-Min
authors.initials: GM
authors.lastname: Do
authors.forename: Eun-Young
authors.initials: EY
authors.lastname: Kwon
authors.forename: Hye-Jin
authors.initials: HJ
authors.lastname: Kim
authors.forename: Seon-Min
authors.initials: SM
authors.lastname: Jeon
authors.forename: Tae-Youl
authors.initials: TY
authors.lastname: Ha
authors.forename: Taesun
authors.initials: T
authors.lastname: Park
authors.forename: Myung-Sook
authors.initials: MS
authors.lastname: Choi
mesh_terms: D000101:Acetyl-CoA C-Acetyltransferase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D001011:Aorta / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics; D043303:Aryldialkylphosphatase / Q000097:blood / Q000378:metabolism; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D002784:Cholesterol / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D025782:Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000201:enzymology; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D000077185:Resveratrol; D013267:Stilbenes / Q000008:administration & dosage*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001057:Apolipoproteins E; D013267:Stilbenes; D017392:Thiobarbituric Acid Reactive Substances; D002784:Cholesterol; D025782:Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent; C506641:Acat1 protein, mouse; D000101:Acetyl-CoA C-Acetyltransferase; D043303:Aryldialkylphosphatase; D000077185:Resveratrol