Effects of an antioxidant-rich juice (sea buckthorn) on risk factors for coronary heart disease in humans.

There is increasing evidence to support the hypothesis that free radical-mediated oxidative processes contribute to atherogenesis. More recently the ability of antioxidant nutrients to affect cell response and gene expression has been reported in vitro, providing a novel mechanistic perspective for the biological activity of antioxidants. Sea buckthorn (Hippophaë rhamnoides L.) is a rich source of antioxidants both aqueous and lipophilic, as well as polyunsaturated fatty acids. The objective of the study was to characterize the antioxidant profile of Sea buckthorn juice (SBJ) and to evaluate its effect on plasma lipids, LDL oxidation, platelet aggregation and plasma soluble cell adhesion protein concentration. Twenty healthy male volunteers were given either a placebo or SBJ for 8 weeks. Additional daily intakes of vitamin C, alpha-tocopherol, beta-carotene and flavonoids through SBJ supplementation were 462, 3.2, 1.0 and 355 mg respectively. There were no significant changes in plasma total cholesterol, LDL-C, platelet aggregation or plasma intercellular cell adhesion molecule 1 (ICAM-1) levels between treatment groups. Although not significant, a 20% and 17% increase in plasma HDL-C and triacylglycerol (TAG) concentrations were observed. SBJ supplementation also resulted in a moderate decrease in the susceptibility of LDL to oxidation.

Effect of genistein and daidzein on platelet aggregation and monocyte and endothelial function.

There has been much recent interest in the cardiovascular benefits of dietary isoflavones. The aim of the present in vitro studies was to investigate potential anti-thrombogenic and anti-atherogenic effects of the isoflavones genistein and daidzein in platelets, macrophages and endothelial cells. Pre-treatment with either isoflavone inhibited collagen-induced platelet aggregation in a dose-dependent manner. In a macrophage cell line (RAW 264.7) activated with interferon gamma plus lipopolysaccharide, both isoflavones were found to inhibit NO production and tumour necrosis factor alpha (TNF-alpha) secretion dose-dependently, but they did not affect mRNA levels for inducible nitric oxide synthase and cyclo-oxygenase-2. Both isoflavones also dose-dependently decreased monocyte chemoattractant protein-1 secretion induced by TNF-alpha in human umbilical vein endothelial cells. Compared with daidzein, genistein exerted greater inhibitory effects for all parameters studied. The present data contributes to our knowledge on the molecular mechanisms by which isoflavones may protect against coronary artery disease. Further studies are required to determine whether the effects of isoflavones observed in the current in vitro studies are relevant to the aetiology of coronary artery disease in vivo.