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Cell hypercholesterolemic

Yu X, Dluz S, Graves DT, et al. Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates. Proc Natl Acad Sci U S A 1992 89(15) 6953-6957. [Pg.224]

Wang-Polagruto JF, Villablanca AC, Polagruto JA, Lee L, Holt RR, Schrader HR, Ensunsa JL, Steinberg FM, Schmitz HH and Keen CL. 2006. Chronic consumption of flavanol-rich cocoa improves endothelial function and decreases vascular cell adhesion molecule in hypercholesterolemic postmenopausal women. J Cardiovasc Pharmacol 47 Suppl 2 S177-186 discussion S206-209. [Pg.175]

High antioxidative activity carvedilol has been shown in isolated rat heart mitochondria [297] and in the protection against myocardial injury in postischemic rat hearts [281]. Carvedilol also preserved tissue GSL content and diminished peroxynitrite-induced tissue injury in hypercholesterolemic rabbits [298]. Habon et al. [299] showed that carvedilol significantly decreased the ischemia-reperfusion-stimulated free radical formation and lipid peroxidation in rat hearts. Very small I50 values have been obtained for the metabolite of carvedilol SB 211475 in the iron-ascorbate-initiated lipid peroxidation of brain homogenate (0.28 pmol D1), mouse macrophage-stimulated LDL oxidation (0.043 pmol I 1), the hydroxyl-initiated lipid peroxidation of bovine pulmonary artery endothelial cells (0.15 pmol U1), the cell damage measured by LDL release (0.16 pmol l-1), and the promotion of cell survival (0.13 pmol l-1) [300]. SB 211475 also inhibited superoxide production by PMA-stimulated human neutrophils. [Pg.885]

Alterations in Cell Surface Glycosphingolipids and Their Metabolism in Familial Hypercholesterolemic Fibroblasts... [Pg.265]

Glycosphingolipid Composition of Normal and Familial Hypercholesterolemic Cells... [Pg.277]

Incorporation of Radioactivity Derived from [3H] Galactose into the Individual Glycosphingolipids of Normal and Familial Hypercholesterolemic Homozygous (FH) Cells Cultured in Fetal Bovine Serum... [Pg.284]

Low Density Lipoprotein Binding and Degradation in Normal, Familial Hypercholesterolemic Homozygous, and Co-cultured Cells... [Pg.286]

Incorporation of radioactivity derived from [%] Galactose into the individual glycosphingolipids of co-cultured normal and familial hypercholesterolemic homozygous cells and a familial hypercholesterolemic heterozygous fibroblast line... [Pg.287]

A low-density lipoprotein binding in normal (A), co-cuhured (O), and familial hyper-cholesterolemic homozygous (A.) cells. B low density lipoprotein degradation in normal (A), co-cuhured (O), and familial hypercholesterolemic homozygous (A) cells... [Pg.288]

Prasad, K., Mantha, S.V., Muir, A.D., and Westcott, N.D. 1998. Reduction of hypercholesterolemic atherosclerosis by CDC-flaxseed with very low alpha-linolenic acid. Atherosclerosis 136, 367-375. Prasad, K., Mantha, S.V., Muir, A.D., and Westcott, N.D. 2000. Protective effect of secoisolariciresinol diglucoside against streptozotocin-induced diabetes and its mechanism. Mol. Cell. Bio-chem. 206, 141-150. [Pg.91]

This chapter summarizes our recent studies on resveratrol, with regard to its effects on(l) oxidation of low-density lipoprotein (LDL), (2) cells effecting development of the AS, and (3) experiments using hypercholesterolemic rabbits. Furthermore, we report preliminary results of the effects of resveratrol in human aortic endothelial cells (HAEC). In these cells, RT-PCR analysis shows that resveratrol elicits an increase in p38 MAP kinase, concomitant with significant induction of heat shock protein 27 (Hsp27). We hypothesize that resveratrol may confer cardioprotection by functioning as a pleiotropic cellular effector. [Pg.146]

The effect different fatty acids have on cholesterolemia is well known. Whatever the kind of the effect (hyper- or hypocholesterolemic), it seems to be more pronounced when the fatty acids are esterified at the inner than at the outer positions of TAGs. The lower hypercholesterolemic effect of saturated fatty acids at the outer positions (64) can be the result of a combination of different factors such as reduced absorption by unabsorbable soap formation, which in turn interferes with cholesterol absorption in the intestinal lumen, partial desaturation and oxidation in the small intestinal cells, and reduced targeting into the fiver (63). The stronger hypocholesterolemic effect of polyunsamrated fatty acids at the i -2-position (65) could be the result of increased influx in the liver (66). [Pg.1905]

R. J. Chan, R. H. BOger. S. M. Bode-B6ger, O. Tangphao. P. S. Tsao, T. F. Blaschke and J. P. Cooke, Asymmetric Dimethylarginine Increases Mononuclear Cell Adhesiveness in Hypercholesterolemic Humans, Arteriosclerosis. Thrombosis, and Va.scular Biology 20 ( 2000) 1040-1056. [Pg.150]


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Hypercholesterolemic

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