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Previously, we demonstrated that in vitro epigallocatechin-3-gallate (EGCG) supplementation inhibited T cell response in mouse spleen cells. In this study, we confirmed this effect of EGCG in mice fed 0.3% EGCG for 6 wk. A coculture with all the combinations of preincubating antigen-presenting cells and T cells with or without EGCG showed that EGCG suppressed antigen-induced T cell proliferation, mainly through a direct effect on T cells. To determine the mechanisms for this effect of EGCG, we stimulated purified mouse T cells with anti-CD3/CD28 in the presence of EGCG (2.5-15 [micro]mol/L) and found that EGCG dose-dependently inhibited cell division and cell cycle progression and this effect of EGCG was more pronounced in [CD4.sup.+] than in [CD8.sup.+] T cells. Interleukin (IL)-2 concentrations in EGCG-treated cell cultures showed no difference up to 24 h but were higher in the cultures at 48 h compared with the untreated control cells. However, intracellular staining showed no difference between EGCG-treated and untreated control cells in IL-2 synthesis, but EGCG-treated cells expressed less IL-2 receptor (IL-2R) compared with untreated control cells. EGCG did not affect mRNA expression of IL-2 and IL-2R. These results indicate that EGCG-induced IL-2 accumulation in 48 h cultures is due to its reduced utilization. In summary, EGCG directly inhibits T cell proliferative response to both polyclonal and antigen-specific stimulation. [CD4.sup.+] cells are more responsive to EGCG than [CD8.sup.+] cells. Future studies should determine the effect of EGCG on [CD4.sup.+] cell subsets to assess its application in T cell-mediated autoimmune diseases. doi: 10.3945/jn.110.124743.

Oats are known to be a healthy food for the heart due mainly to their high [beta]-glucan content. In addition, they contain more than 20 unique polyphenols, avenanthramides, which have shown strong antioxidant activity in vitro and in vivo. The polyphenols of oats have also recently been shown to exhibit anti-inflammatory, antiproliferative, and anti-itching activity, which may provide additional protection against coronary heart disease, colon cancer, and skin irritation. [c] 2009 International Life Sciences Institute doi: 10.1111/j.1753-4887.2009.00256.x

Angiogenesis is necessary for the growth of adipose tissue. Dietary polyphenols may suppress growth of adipose tissue through their antiangiogenic activity and by modulating adipocyte metabolism. We investigated the effect of curcumin, the major polyphenol in turmeric spice, on angiogenesis, adipogenesis, differentiation, apoptosis, and gene expression involved in lipid and energy metabolism in 3T3-L1 adipocyte in cell culture systems and on body weight gain and adiposity in mice fed a high-fat diet (22%) supplemented with 500 mg curcumin/kg diet for 12 wk. Curcumin (5-20 [micro]mol/L) suppressed 3T3-L1 differentiation, caused apoptosis, and inhibited adipokine-induced angiogenesis of human umbilical vein endothelial cells. Supplementing the high-fat diet of mice with curcumin did not affect food intake but reduced body weight gain, adiposity, and microvessel density in adipose tissue, which coincided with reduced expression of vascular endothelial growth factor (VEGF) and its receptor VEGFR-2. Curcumin increased 5'AMP-activated protein kinase phosphorylation, reduced glycerol-3-phosphate acyl transferase-1, and increased carnitine palmitoyltransferase-1 expression, which led to increased oxidation and decreased fatty acid esterification. The in vivo effect of curcumin on the expression of these enzymes was also confirmed by real-time RT-PCR in subcutaneous adipose tissue. In addition, curcumin significantly lowered serum cholesterol and expression of PPAR[gamma], and CCAAT/enhancer binding protein [alpha], 2 key transcription factors in adipogenesis and lipogenesis. The curcumin suppression of angiogenesis in adipose tissue together with its effect on lipid metabolism in adipocytes may contribute to lower body fat and body weight gain. Our findings suggest that dietary curcumin may have a potential benefit in preventing obesity.

Polymorphisms in genes involved in vitamin E uptake, distribution, metabolism, and molecular action may be important determinants for the protective effects of vitamin E supplementation. The haptoglobin 2-2 polymorphism is associated with increased production of oxygen free radicals and reduces levels of vitamin E and C; the consequent elevated risk for cardiovascular disease can be prevented by vitamin E supplementation.

We used high-density oligonucleotide arrays to measure transcriptional alterations in the heart and brain (neocortex) of 30-mo-old B6C3[F.sub.1] mice supplemented with [alpha]-tocopherol ([alpha]T) and [gamma]-tocopherol ([gamma]T) since middle age (15 mo). Gene expression profiles were obtained from 5- and 30-mo-old control mice and 30-mo-old mice supplemented with [gamma]T (1 g/kg) or a mixture of [alpha]]T and [gamma]T (500 mg/kg of each tocopherol) from middle age (15 too). In the heart, both tocopherol-supplemented diets were effective in inhibiting the expression of genes previously associated with cardiomyocyte hypertrophy and increased innate immunity. In the brain, induction of genes encoding ribosomal proteins and proteins invorved in ATP biosynthesis was observed with aging and was markedly prevented by the mixture of [alpha]T and [gamma]T supplementation but not by [alpha]T alone. These results demonstrate that middle age-onset dietary supplementation with [alpha]T and [gamma]T can partially prevent age-associated transcriptional changes and that these effects are tissue and tocopherol specific.

Impairment of endothelium-dependent vasodilation is associated with the initiation and development of atheroscierosis. Vasodilator prostanoids constitute a protective mechanism in maintaining normal vasomotor function. In the current study, we determined the effect of in vitro vitamin E supplementation at physiologically relevant concentrations (10-60 [micro]mol/L) on the production of the vasodilator prostanoids prostaglandin [I.sub.2] (PG[I.sub.2]; prostacyclin) and prostaglandin [E.sub.2] (PG[E.sub.2]) by human aortic endothelial cells (HAECs) as well as its underlying mechanism. Results showed that vitamin E dose dependently (10-40 [micro]mol/L) increased the production of both prostanoids by HAECs. This was associated with a dose-dependent (10-40 [micro]mol/L) upregulation of cytosolic phospholipase [A.sub.2] (cPL[A.sub.2]) expression and arachidonic acid release. In contrast, vitamin E dose dependently (10-60 [micro]mol/L) inhibited cyclooxygenase (COX) activity but did not affect the expression of either COX-1 or COX-2, indicating that the effect of vitamin E on COX activity was post-translational. Thus, vitamin E had opposing effects on the 2 key enzymes in prostanoid biosynthesis; at the concentrations used in this study, this resulted in a net increase in the production of vasodilator prostanoids. The vitamin E-induced increase in PG[I.sub.2] and PG[E.sub.2] production may contribute to its suggested beneficial effect in preserving endothelial function. J. Nutr. 135: 1847-1853, 2005. KEY WORDS: * vitamin E * human aorta endothelial cells * prostanoids * cyclooxygenase * phospholipase [A.sub.2]

Overweight and obese are major health concerns owing to the complex co-morbidities that inevitably follow. Diet and exercise are the primary means by which people attempt to lose weight. A recent study in an obese mouse model suggested that angiogenesis inhibitors, which are designed to inhibit tumor growth, are able to reduce adipose tissue mass by cutting off the blood supply. This approach may have application in the prevention and treatment of obesity by using foods with antiangiogenic potential. Key words: angiogenesis, adipose tissue, obesity, angiogenesis inhibitor

Expression of adhesion molecules on the surface of endothelial and immune cells is important for the interaction between immune and endothelial cells during the inflammatory process. Several of these adhesion molecules have been identified and are believed to be important in the pathogenesis of atherosclerosis. The soluble forms of adhesion molecules are shed from cell surfaces and released into blood circulation; their measurement may have use as markers in predicting cardiovascular disease. Experimental and some clinical data have indicated that reducing expression of some adhesion molecules is another mechanism by which dietary fats such as n-3 polyunsaturated fatty acids and oleic acid, as well as vitamin E and other antioxidants found in fruits and vegetables, may lower the risk of cardiovascular disease. Key Words: soluble adhesion molecules, atherosclerosis, n-3 PUFA, oleic acid, vitamin E

This article discusses the relationship between vitamin E and the progression of atherosclerosis. Topics include cardiovascular disease prevention, low density lipoproteins, and health aspects of antioxidants.

Research presented concerns the suggestion that the omega-3 poly-unsaturated fatty acids found in fish oil provide a measure of protection against cardiovascular disease. Research examines the relationship between fish oil supplementation and vascular inflammation.

Aging is associated with a decline in the immune response in mammals. Conjugated linoleic acid (CLA) has been suggested to have immunoenhancing properties. We examined the influence of dietary CLA on the immune response of young and old mice. Forty young (4 mo) and 40 old (22 mo) mice consumed ad libitum diets containing 0 or 1 g CLA/100 g for 8 wk. Splenocytes from half of the mice were isolated to evaluate proliferation to concanavalin A (Con A) (0.5, 1.5, 5.0 mg/L) and phytohemagglutinin A (PHA) (5, 20, 40 mg/L) and lipopolysaccharide (LPS) (5, 15, 30 mg/L), natural killer cell (NK) activity and prostaglandin (PG)[E.sub.2] and interleukin (IL)-2 production. The remaining mice were used to evaluate in vivo delayed-type hypersensitivity (DTH) skin response. There was a significant decline due to age in response to all three mitogens tested (P < 0.05). CLA supplementation significantly increased all CLA isomers measured in hepatic neutral lipids and phospholipids (P < 0.05). Young mice fed 1% CLA had greater splenocyte proliferation in response to Con A (0.5 and 5.0 mg/L) and PHA (40 mg/L) (P < 0.05) than young mice fed control diet. Old mice fed 1 g CLA/100 g had significantly higher proliferative response to optimal concentrations of Con A (1.5 mg/L) (P < 0.001) than the mice fed the control diet. Old mice fed the control diet had significantly lower splenocyte IL-2 production than the young mice (P < 0.005). CLA-supplemented young mice had significantly higher splenocyte IL-2 production than those fed the control diet (P < 0.05). CLA had no effect on NK cell activity, PG[E.sub.2] production or DTH in young or old mice. Further studies are needed to determine the mechanism of CLA-induced enhancement of IL-2 production and T cell proliferation. KEY WORDS: conjugated linoleic acid; mice; immune response; age

Marine-derived (n-3) polyunsaturated fatty acids (PUFAs) and vitamin E appear to be the best nutrients to effect a reduction in the risk of cardiovascular disease and decrease the development of atherosclerosis. The beneficial effects are linked to action at tissue, cellular and molecular levels.