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United States Department of Agriculture

Agricultural Research Service

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Location: Jean Mayer Human Nutrition Research Center On Aging

Project Number: 1950-51000-058-04-S
Project Type: Specific Cooperative Agreement

Start Date: Oct 1, 2006
End Date: Sep 30, 2011

LAB:Vascular biology Determine at molecular and cellular levels the mechanisms by which the antioxidant components of foods (vitamins E, carotenoids, and polyphenols such as catechins) singly and interactively modulate development of atherosclerosis and angiogenesis. Determine the effect of components of foods-vitamin E, carotenoids, lipids and polyphenols such as catechins, as well as their synergistic interactions in preventing and in reducing the risk of atherosclerosis, specifically when they are incorporated into the diet of animal models early in life compared to middle and later ages.

LAB:Vascular Biology The effect of mixed tocopherols at the concentrations commonly found in human plasma and after vitamin E supplementation will be examined in a cell culture system for modulation of immune and endothelial cell interaction and inflammatory cytokines. In this system, the interaction of vitamin E with avenanthramide, a flavonoid found in oats, will be also tested for anti-atherogenic and anti-inflammatory action. The molecular mechanism of green tea catechins' inhibition of angiogenesis will be tested in a cell culture system using Matrigel and 3D gel. This effect of green tea will be investigated in vivo using the Matrigel plug assay in young and aged mice. The effect of vitamin E supplementation started from early, middle, and late age on the inhibition of atherosclerosis will be determined in LDL receptor null mice, which will be fed medium or high fat/cholesterol diets. The potential inhibitory effect of dietary vitamin E on the inhibition of atherosclerosis will be further tested in mice models when vitamin E is combined with lycopene, a carotenoid found in tomato, and with epigallocatechin gallate, the major catechin of green tea.

Last Modified: 2/23/2016
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