135 research outputs found
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Vitamin E inhibits CD36 scavenger receptor expression in hypercholesterolemic rabbits
No full textA numerous studies suggest that Vitamin E has a preventive role in atherosclerosis, although the mechanism of action still remains unclear. CD36, a member of the scavenger receptor family is centrally involved in the uptake of oxidized low density proteins (oxLDLs) from bloodstream. During the atherosclerotic process, the lipid cargo of oxLDL accumulates in macrophages and smooth muscle cells, inducing their pathological conversion to foam cells. In the present study, we investigate the role of Vitamin E on CD36 expression in an in vivo model. Atherosclerosis was induced by a 2% cholesterol containing Vitamin E poor diet. Three groups of six rabbits each were studied. The first group (control) was fed on Vitamin E poor diet. The second group was fed with Vitamin E poor diet containing 2% cholesterol and the rabbits in the third group were fed with Vitamin E poor diet containing 2% cholesterol and received injections of 50 mg/kg of Vitamin E i.m. After 4 weeks, aortas were removed and analysed by light microscopy for atherosclerotic lesions. Aortic samples were analysed for CD36 mRNA expression. The aortas of cholesterol-fed rabbits showed typical atherosclerotic lesions, detected by macroscopic and microscopic examination, and exhibited an increase in CD36 mRNA expression. Vitamin E fully prevented cholesterol induced atherosclerotic lesions and the induction of CD36 mRNA expression. The effects observed at the level of CD36 scavenger receptor expression in vivo suggest an involvement of reduced foam cell formation in the protective effect of Vitamin E against atherosclerosis
Vitamin E attenuates homocysteine and cholesterol induced damage in rat aorta
No full textBackground: The aim of this study was to investigate the effect of vitamin E on homocysteine and cholesterol-induced damage of rat aorta. Methods: Wistar rats (all fed with a vitamin E poor diet) were divided into five groups. Control group was fed with the diet only, the second group received 1 mg kg(-1) day(-1) L-methionine in drinking water, the third group was fed with 2% cholesterol containing diet, the fourth group received L-methionine and cholesterol together, and the fifth group was fed with L-methionine and cholesterol and received intramuscular injections of vitamin E. After 4 weeks serum homocysteine, cholesterol and vitamin E levels were measured; aortas were removed; collagen and elastin and the major extracellular matrix components were evaluated microscopically as indicators of aortic degeneration. Aortic collagen content was measured by a colorimetric hydroxyproline assay. Results: Four-week diet supplementation with methionine and cholesterol caused a twofold increase in serum homocysteine and 22% increase in serum cholesterol levels; endothelial damage and degenerative alterations in the aortic media were observed, as indicated by the dissociation of elastic fibers and accumulation of collagen. Vitamin E completely prevented the accumulation of collagen and largely prevented aorta damage as shown by the morphological data. Conclusion: The results indicate that, even moderate increases in homocysteine and cholesterol levels are sufficient to induce vascular degeneration that may be prevented by vitamin E supplementation. (C) 2013 Elsevier Inc. All rights reserved
Expression of cell cycle proteins in cortical neurons—Correlation with glutamate‐induced neurotoxicity
No full textThe effect of the north-east ice stream on the Greenland ice sheet in changing climates
No full textThe north-east Greenland ice stream (NEGIS) was discovered as a large fast-flow feature of the Greenland ice sheet by synthetic aperture radar (SAR) imaginary of the ERS-1 satellite. In this study, the NEGIS is implemented in the dynamic/thermodynamic, large-scale ice-sheet model SICOPOLIS (Simulation Code for POLythermal Ice Sheets). In the first step, we simulate the evolution of the ice sheet on a 10-km grid for the period from 250 ka ago until today, driven by a climatology reconstructed from a combination of present-day observations and GCM results for the past. We assume that the NEGIS area is characterized by enhanced basal sliding compared to the "normal", slowly-flowing areas of the ice sheet, and find that the misfit between simulated and observed ice thicknesses and surface velocities is minimized for a sliding enhancement by the factor three. In the second step, the consequences of the NEGIS, and also of surface-meltwater-induced acceleration of basal sliding, for the possible decay of the Greenland ice sheet in future warming climates are investigated. It is demonstrated that the ice sheet is generally very susceptible to global warming on time-scales of centuries and that surface-meltwater-induced acceleration of basal sliding can speed up the decay significantly, whereas the NEGIS is not likely to dynamically destabilize the ice sheet as a whole
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The effect of tocopheryl phosphates on atherosclerosis progression in rabbits fed with a high cholesterol diet
No full textThe effect of tocopheryl phosphate on atherosclerosis progression has been studied in rabbits, fed with a 2% cholesterol diet and compared with an equivalent amount of alpha-tocopheryl acetate. The results show that the atherosclerotic-preventing effect of the phosphate derivative was more pronounced than that of the acetate derivative. alpha-Tocopheryl phosphate was also more potent in diminishing the expression of CD36 than the acetate derivative
Molecular mechanisms of cholesterol or homocysteine effect in the development of atherosclerosis: Role of vitamin E
No full textThe effect of tocopheryl phosphates on atherosclerosis progression in rabbits fed with a high cholesterol diet
No full textThe effect of tocopheryl phosphate on atherosclerosis progression has been studied in rabbits, fed with a 2% cholesterol diet and compared with an equivalent amount of alpha-tocopheryl acetate. The results show that the atherosclerotic-preventing effect of the phosphate derivative was more pronounced than that of the acetate derivative. alpha-Tocopheryl phosphate was also more potent in diminishing the expression of CD36 than the acetate derivative. (c) 2006 Elsevier Inc. All rights reserved
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Molecular mechanism of alpha-tocopheryl-phosphate transport across the cell membrane
No full textalpha-Tocopheryl-phosphate (alpha-TP) is synthesized and hydrolyzed in animal cells and tissues where it modulates several functions. alpha-TP is more potent than alpha-T in inhibiting cell proliferation, down-regulating CD36 transcription, inhibiting atherosclerotic plaque formation. Administration of alpha-TP to cells or animals requires its transfer through membranes, via a transporter. We show here that alpha-TP is passing the plasma membrane via a system that is inhibited by glibenclamide and probenecid, inhibitors of a number of transporters. Glibenclamide and probenecid prevent dose-dependently alpha-TP inhibition of cell proliferation. The two inhibitors act on ATP binding cassette (ABC) and organic anion transporters (OAT). Since ABC transporters function to export solutes and alpha-TP is transported into cells, it may be concluded that alpha-TP transport may occur via an OAT family member. Due to the protection by glibenclamide and probenecid on the alpha-TP induced cell growth inhibition it appears that alpha-TP acts after its uptake inside cells
Cell cycle markers have different expression and localization patterns in neuron-like PC12 cells and primary hippocampal neurons
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