Dietary Wine Phenolics Catechin, Quercetin, and Resveratrol Efficiently Protect Hypercholesterolemic Hamsters against Aortic Fatty Streak Accumulation
The effects of the phenolic compounds catechin (Cat), quercetin (Qer), and resveratrol (Res) present in red wine on early atherosclerosis were studied in hamsters. Hamsters (n = 32) were divided into 4 groups of 8 and fed an atherogenic diet for 12 weeks. They received by force-feeding 7.14 mL/(kg of body wt.day) Cat, Qer, or Res in water [2.856 mg/(kg of body wt.day) for Cat and 0.1428 mg/(kg of body wt.dday) for Qer and Res], mimicking a moderate consumption of alcohol-free red wine (equivalent to that supplied by the consumption of about two glasses of red wine per meal for a 70 kg human), or water as control. Plasma cholesterol concentration was lower in groups that consumed phenolics than in controls. The increase in plasma apolipoprotein (Apo) A1 concentration was mainly due to Cat (26%) and Qer (22%) and to a lesser extent, but nonsignificantly, Res (19%). Apo-B was not affected. Plasma antioxidant capacity was not improved, and there was no sparing effect on plasma vitamins A and E. Plasma iron and copper concentrations were not modified nor were liver super oxide dismutase and catalase activities. A sparing effect of Qer on liver glutathione peroxidase activity appeared, whereas Cat and Res exhibited a smaller effect. Aortic fatty streak area was significantly reduced in the groups receiving Cat (84%) or Qer (80%) or Res (76%) in comparison with the controls. These findings demonstrate that catechin, quercetin, and resveratrol at nutritional doses prevent the development of atherosclerosis through several indirect mechanisms.
Available from: Isabella Montenegro Brasil
- "Phytochemicals, especially phenolic compounds, exhibit great in vitro and in vivo antioxidant potential, and their beneficial effects are extensively reported in models involving oxidative stresses caused by hypercholesterolemic and atherogenic diets, for example (Auger et al., 2005; Décordé et al., 2008). These bioactive compounds are able to scavenge radical oxygen species (ROS) and consequently reduce oxidative cell damage (Spormann et al., 2008). "
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ABSTRACT: Fruits are a rich source of a variety of biologically active compounds that can have complementary and overlapping mechanisms of action, including detoxification, enzyme modulation and antioxidant effects. Although the effects of tropical fruits have been examined individually, the interactive antioxidant capacity of the bioactive compounds in these formulations has not been sufficiently explored. For this reason, this study investigated the effect of two tropical fruit juices (FA and FB) on lipid peroxidation and antioxidant enzymes in rats. Seven groups, with eight rats each, were fed a normal diet for 4weeks, and were force-fed daily either water (control), 100, 200, or 400mg of FA or FB per kg. The results showed that the liver superoxide dismutase and catalase activities (FA200), erythrocytes glutathione peroxidase (FB400) and thiobarbituric acid-reactive substances (FB100, FA400, FB200, FB400) were efficiently reduced by fruit juices when compared with control; whereas HDL-c increased (FB400).
Food Chemistry 08/2014; 157C:179-185. DOI:10.1016/j.foodchem.2014.01.090 · 3.39 Impact Factor
Available from: Ramaroson Andriantsitohaina
- "Interestingly, quercetin is more effective than others flavonoids in the prevention of atherosclerosis . While quercetin has no beneficial effects on the plasma lipid profile  , it inhibits significantly the susceptibility of LDL to oxidation , the oxidized-LDL-induced cytotoxicity  and the aortic fatty streak formation . "
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ABSTRACT: Cardiovascular diseases are an important public health problem because they represent a major cause of death worldwide. The pathophysiology of these chronic diseases is defined, among others, by an excess of reactive oxygen species production, a defect of endothelium-dependent vasodilation, a high blood pressure or a modification of platelet function. Epidemiological studies suggest that the beneficial cardiovascular health effects of diets rich in fruits and vegetables are, in part, mediated by their flavonoid content, with particular benefits provided by members of this family such as epigallocatechin gallate, quercetin or delphinidin. Many studies show that these phytochemicals are promising natural compounds to prevent cardiovascular diseases associated with endothelial dysfunction. Mechanistically, short-term effects on endothelium-dependent vasodilation following the consumption of these flavonoids have been linked to an increased nitric oxide bioactivity. Moreover, besides their well-described antioxidant properties, these flavonoids are able to prevent endothelial cell apoptosis and to modulate various signaling pathways leading to inflammation. Therefore, this review attempts to outline our understanding about the pleiotropic beneficial effects of epigallocathecin gallate, quercetin or delphinidin on cardiovascular diseases associated with endothelial dysfunction. Furthermore, this review aims to identify the potential protective vascular effects of these flavonoids and their therapeutic value in cardiovascular medicine.
Cardiovascular & hematological agents in medicinal chemistry 03/2014; 11(4). DOI:10.2174/1871525712666140309233048
Available from: Jelver Alexander Sierra restrepo
- "1–5), suggesting that the effects of quercetin on macrophages might be operating in vivo and could explain at least some of the atheroprotective activities of this flavonoid. Our results are in line with previous reports showing atheroprotective effects of oral quercetin in various animal models (Hayek et al., 1997; Auger et al., 2005; Juz´wiak et al., 2005; Leckey et al., 2010; Loke et al., 2010; Kleemann et al., 2011) and further extend them by demonstrating a significant level of protection after intraperitoneal chronic administration. Furthermore, we demonstrated reduced inflammatory macrophage and T cell infiltrate in the atheromatous plaque (Fig. 6), which could have been a consequence of the antioxidant/anti-inflammatory activity of quercetin on macrophages (Figs. 4 and 5). "
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ABSTRACT: Many studies have demonstrated that the flavonoid quercetin protects against cardiovascular disease (CVD) and related risk factors. Atherosclerosis, the underlying cause of CVD, is also attenuated by oral quercetin administration in animal models. Although macrophages are key players during fatty streak formation and plaque progression and aggravation, little is known about the effects of quercetin on atherogenic macrophages. Here, we report that primary bone marrow-derived macrophages internalized less oxidized low-density lipoprotein (oxLDL) and accumulated less intracellular cholesterol in the presence of quercetin. This reduction of foam cell formation correlated with reduced surface expression of the oxLDL receptor CD36. Quercetin also targeted the lipopolysaccharide-dependent, oxLDL-independent pathway of lipid droplet formation in macrophages. In oxLDL-stimulated macrophages, quercetin inhibited reactive oxygen species production and interleukin (IL)-6 secretion. In a system that evaluated cholesterol crystal-induced IL-1β secretion via nucleotide-binding domain and leucine-rich repeat containing protein 3 inflammasome activation, quercetin also exhibited an inhibitory effect. Dyslipidemic apolipoprotein E-deficient mice chronically treated with intraperitoneal quercetin injections had smaller atheromatous lesions, reduced lipid deposition, and less macrophage and T cell inflammatory infiltrate in the aortic roots than vehicle-treated animals. Serum levels of total cholesterol and the lipid peroxidation product malondialdehyde were also reduced in these mice. Our results demonstrate that quercetin interferes with both key proatherogenic activities of macrophages, namely foam cell formation and pro-oxidant/proinflammatory responses, and these effects may explain the atheroprotective properties of this common flavonoid.
Journal of Pharmacology and Experimental Therapeutics 08/2012; 343(2):296-306. DOI:10.1124/jpet.112.196147 · 3.97 Impact Factor
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