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Anti-atherosclerosis

The oxidized LDL might damage cells which connect the blood vessel walls by stimulating numerous responses including inflammation, smooth muscle cell proliferation and clotting mechanisms, all of which might lead to atherosclerosis. [Pg.34]

The antiatherosclerotic effect of proanthocyanidin-rich grape seed extracts was examined in cholesterol-fed rabbits. The proanthocyanidin-rich extracts [0.1% and 1% in diets (w/w)] did not change the serum lipid profile, but reduced the level of the cholesteryl ester hydroperoxides (ChE-OOH) induced by 2,2/-azo-bis(2-amidinopropane-dihydrochloride (AAPH), the aortic malonaldehyde (MDA) content and severe atherosclerosis. The immuno-histochemical analysis revealed a decrease in the number of the oxidized LDL-positive macrophage-derived foam cells on the atherosclerotic lesions of the aorta in the rabbits fed the proanthocyanidin-rich extract. When the proanthocyanidin-rich extract was administered orally to the rats, proantho-cyanidin was detected in the plasma. In an in vitro experiment using human plasma, the addition of the proanthocyanidin-rich extract to the plasma inhibited the oxidation of cholesteryl linoleate in the LDL, but not in the LDL isolated after the plasma and the extract were incubated in advance. From these results, proanthocyanidins of the major polyphenols in red wine might trap ROSs in the plasma and interstitial fluid of the arterial wall, and consequently display antiatherosclerotic activity by inhibiting the oxidation of the LDL [92]. [Pg.36]

The polyphenols such as anthocyanidins might have a protective effect on atherosclerosis. This concept suggests that the Recommended Optimal Intake (ROI) is a more important factor for the antioxidation than the Recommended Dietary Allowance (RDA). Now, considering the absence of the appropriate methodology to identify anthocyanidins in the plasma, the analysis of the plasma antioxidant capacity might be a suitable index to define the optimal nutritional intake [95]. [Pg.37]

there are many evidences, which support the cardioprotective effects of red wine. These cardioprotective properties of wine might have [Pg.37]


Day CE, Stafford WW, Schurr PE (1977) Utility of a selected line (SEA) of the Japanese quail (Cotumix coturnix japonica) for the discovery of new anti-atherosclerosis drugs. Anim Sci 27 817-821... [Pg.189]

Fatty acids with two or more conjugated double bonds are found in some plants and animals. In tissues of ruminant animals (and, hence, in meat and dairy products), fatty acids with conjugated diene system were detected as intermediates or by-products in the biohydrogenation of linoleic acid by microorganisms in the rumen. The main isomer, 9-cis, ll-fran -octadecadienoic acid, may account for up to 1% of the total fatty acids of milk fat. 9-cis, ll-fran5-15-cw-octadecatrienoic acid, derived from a-linolenic acid, is present in ruminant tissues only in trace levels. This fatty acid has been shown to have several medical properties, especially anti-cancer and anti-atherosclerosis effects. [Pg.944]

Pasceri V, Chang J, Willerson PT, Yeh ETH. Modulation of C-reactive protein-mediated monocyte chemoattractant protein-1 induction in human endothelial cells by anti-atherosclerosis drugs. Circulation 2001 103 2531-34. [Pg.286]

Perhaps the most successful anti-atherosclerosis medications are the statins. These drugs bind to HMG-CoA reductase and directly inhibit its activity, thereby lowering cholesterol biosynthesis and the pool of hepatic cholesterol. Activation of SREBP in response to this cholesterol depletion promotes increased synthesis of HMG-CoA reductase and the LDL receptor. Of most Importance here is the resulting increased numbers of hepatic LDL receptors, which can mediate increased import of LDL cholesterol from the plasma. Statins also appear to inhibit atherosclerosis by suppressing the inflammation that triggers the process. Although the mechanism of this Inhibition is not well understood, it apparently contributes to the atheroprotec-tive effect of statins. [Pg.773]

Resin based on diglycidyl ester of hexahydrophthalic acid. Has anti-atherosclerosis properties, insect attractant activity Synonyms Araldit CY 184 1,2-cyclohexanedicarboxylic acid bis(2,3-epoxypropyl) ester 1,2-cyclohexanedicarboxylic acid bis(oxir-anylmethyl) ester 1,2-cyclohexanedicarboxylic acid diglycidyl ester cycloaliphatic glycidyl ester bis(oxiranylmethyl)-i,2-cyclohex-anedicarboxylic acid... [Pg.1213]

Orekhov AN, Tertov VV, Sobenin lA, Pivovarova EM (1995) Direct anti-atherosclerosis-related effects of garlic. Ann Med 27(l) 63-65... [Pg.3694]

Ni W, Egashira K, Kitamoto S, et al. New anti-monocyte chemoattractant protein-1 gene therapy attenuates atherosclerosis in apolipoprotein E-knockout mice. Circulation 2001 103(16) 2096-2101. [Pg.232]

Various antibody preparations have been developed that facilitate imaging of vascular-related conditions, including myocardial infarction, deep vein thrombosis and atherosclerosis. Anti-myosin monoclonal antibody fragments (Fab) labelled with mIn, for example, have been used for imaging purposes in conjunction with a planar gamma camera. The antibody displays specificity for intracellular cardiac myosin, which is exposed only upon death of heart muscle tissue induced by a myocardial infarction (heart attack). [Pg.395]

A high plasma concentration of LDL (usually measured as LDL-cholesterol) is a risk factor for the development of atheroma whereas a high concentration of HDL is an anti-risk factor for cardiovascular disease (CVD). Fundamental discoveries relating to cholesterol metabolism and the importance of the LDL receptor made by Nobel laureates Joseph Goldstein and Michael Brown led to an understanding of the role of LDL in atherosclerosis. The impact of HDL in reducing CVD risk is often explained by the removal of excess cholesterol from tissues and its return to the liver, a process known as reverse cholesterol transport. However, evidence from research by Gillian Cockerill and others shows that HDL has a fundamental anti-inflammatory role to play in cardioprotection. [Pg.165]

Yoshii T, Iwai M, Li Z, Chen R, Ide A, Fnknnaga S, Oshita A, Mogi M, Higaki J, Horinchi M. (2006) Regression of atherosclerosis by amlodipine via anti-inflammatory and anti-oxidative stress actions. Hypertens Res 29 457 66. [Pg.221]

Nakano K, Egashira K, Ohtani K, Gang Z, Iwata E, Miyagawa M, Sunagawa K. (2008) Azelnidipine has anti-atherosclerotic effects independent of its blood pressure-lowering actions in monkeys and mice. Atherosclerosis 196 172-179. [Pg.221]


See other pages where Anti-atherosclerosis is mentioned: [Pg.187]    [Pg.215]    [Pg.124]    [Pg.384]    [Pg.34]    [Pg.1775]    [Pg.367]    [Pg.771]    [Pg.19]    [Pg.2961]    [Pg.3218]    [Pg.128]    [Pg.143]    [Pg.91]    [Pg.187]    [Pg.215]    [Pg.124]    [Pg.384]    [Pg.34]    [Pg.1775]    [Pg.367]    [Pg.771]    [Pg.19]    [Pg.2961]    [Pg.3218]    [Pg.128]    [Pg.143]    [Pg.91]    [Pg.124]    [Pg.162]    [Pg.139]    [Pg.108]    [Pg.215]    [Pg.219]    [Pg.40]    [Pg.264]    [Pg.313]    [Pg.315]    [Pg.319]    [Pg.320]    [Pg.406]    [Pg.182]    [Pg.183]    [Pg.185]    [Pg.71]    [Pg.73]    [Pg.259]    [Pg.311]    [Pg.11]   
See also in sourсe #XX -- [ Pg.34 ]




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