Inhibitory effects of vitamin E on endothelial‐dependent adhesive interactions with leukocytes induced by oxidized low density lipoprotein

Yoshida, Norimasa; Manabe, Hiroki; Terasawa, Yoshimitsu; Nishimura, Hiroshi; Enjo, Fumio; Nishino, H.; Yoshikawa, Toshikazu

doi:10.1002/biof.5520130142

Cited by 34 publications

(26 citation statements)

References 28 publications

(26 reference statements)

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“…pherol decreased the expression of CD11b/CD18 on human neutrophils and monocytes induced by oxLDL in both in vitro and ex vivo studies [2][3][4]. These data support that vitamin E supplementation may reduce the extent of the oxLDL-induced monocyte-endothelial interaction and, thus, be protective against atherosclerosis.…”

supporting

confidence: 59%

Tocotrienols and Atherosclerosis

Naito

Shimozawa

Yoshikawa

2004

J. Clin. Biochem. Nutr.

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Summary The adherence of monocytes to the vascular endothelial cells is an important early event in atherogenesis. Monocyte adherence to endothelial cells is induced by oxidized low density lipoprotein (LDL) and mediated by multiple cell adhesion molecules including vascular cell-adhesion molecule 1 (VCAM-1). Enhanced endothelial expression of these molecules by oxidized LDL has been shown to be a critical step in foam cell formation and the development of atherosclerosis. Recent studies have demonstrated that vitamin E inhibited the expression of mRNA and protein for VCAM-1 by endothelial cells in rienol was a potent and effective agent for the reduction of cellular VCAM-1 expression and monocytic cell adherence. The inhibitory effects of vitamin E analogs on the adhesiveness of endothelial cells correlated with their intracellular concentrations. Anti-atherogenic effects of tocotrienols may be derived from their properties of cholesterol-lowering effect, protein kinase C inhibition, and modulation of cyclooxygenase cascade. Although recent human studies have raised some doubts on the efficacy of vitamin E in the prevention of progression of atherosclerotic lesions, the experimental studies using tocotrienol strongly support its positive effect on the reduction of risk of atherogenesis.Further studies will be necessary for clarifying the anti-atherogenic effect of tocotrienol and its bioavailability after oral administration.

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supporting

confidence: 59%

Tocotrienols and Atherosclerosis

Naito

Shimozawa

Yoshikawa

2004

J. Clin. Biochem. Nutr.

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“…␣-Tocopherol is believed to have a cytoprotective effect, which is attributed to its ability to prevent leukocyte-endothelial interactions (27)(28)(29), and to act as a scavenger of highly reactive oxygen radicals in various pathophysiological processes (30,31). ␣-Tocopherol protects against apoptosis not only by scavenging reactive oxygen species, but also by inhibiting caspase activity, which means that its activity may exceed that of a mere antioxidant (22).…”

Section: Discussionmentioning

confidence: 99%

Effects of Genistein on Oxidative Injury in Endothelial Cells

Huang

Liu

Chang

et al. 2008

J Nutr Sci Vitaminol

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SummaryThe aim of this study was to test the hypothesis that genistein protects vascular endothelial cells against the pro-atherosclerotic stressor, oxidized low-density lipoprotein (ox-LDL), by inducing antioxidant enzymes and preventing apoptosis. Human umbilical cord-derived endothelial cells (ECV 304) were incubated with genistein (10-100 mol/L), the radical scavenging antioxidant vitamin E ( ␣ -tocopherol, 50 mol/L), or vehicle for 24 h and then were incubated with ox-LDL for an additional 24 h. Subsequently, antioxidant enzyme activities, lipid peroxidation, adhesion to monocytes, cell morphology, viability and apoptotic index were assessed. Ox-LDL decreased superoxide dismutase and glutathione peroxidase activities in endothelial cells and caused lipid peroxidation, adhesion to monocytes, morphological injury and apoptosis ( p Ͻ 0.05). These effects were prevented by vitamin E and dose-dependently by genistein ( p Ͻ 0.05). Further, this effect of genistein is associated with maintenance of antioxidant enzyme activities and inhibition of lipid peroxidation.

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“…Studies carried out on cultures of endothelial cells treated with oxLDL have shown an increase at the levels of gene and protein expression of ICAM and VCAM-1 adhesion molecules [89]. Previous treatment with -tocopherol reduced the endothelial cellular adhesion proteins expression.…”

Section: Genesmentioning

confidence: 98%

Anti‐atherosclerotic effects of vitamin E – myth or reality?

Munteanu

Zingg

Azzi

2004

J Cellular Molecular Medi

127

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Atherosclerosis and its complications such as coronary heart disease, myocardial infarction and stroke are the leading causes of death in the developed world. High blood pressure, diabetes, smoking and a diet high in cholesterol and lipids clearly increase the likelihood of premature atherosclerosis, albeit other factors, such as the individual genetic makeup, may play an additional role. Several epidemiological studies and intervention trials have been performed with vitamin E, and some of them showed that it prevents atherosclerosis. For a long time, vitamin E was assumed to act by decreasing the oxidation of LDL, a key step in atherosclerosis initiation. However, at the cellular level, vitamin E acts by inhibition of smooth muscle cell proliferation, platelet aggregation, monocyte adhesion, oxLDL uptake and cytokine production, all reactions implied in the progression of atherosclerosis. Recent research revealed that these effects are not the result of the antioxidant activity of vitamin E, but rather of precise molecular actions of this compound. It is assumed that specific interactions of vitamin E with enzymes and proteins are at the basis of its non-antioxidant effects. Vitamin E influences the activity of several enzymes (e.g. PKC, PP2A, COX-2, 5-lipooxygenase, nitric oxide synthase, NADPHoxidase, superoxide dismutase, phopholipase A2) and modulates the expression of genes that are involved in atherosclerosis (e.g. scavenger receptors, integrins, selectins, cytokines, cyclins). These interactions promise to reveal the biological properties of vitamin E and allow designing better strategies for the protection against atherosclerosis progression.

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Inhibitory effects of vitamin E on endothelial‐dependent adhesive interactions with leukocytes induced by oxidized low density lipoprotein

Cited by 34 publications

References 28 publications

Tocotrienols and Atherosclerosis

Tocotrienols and Atherosclerosis

Effects of Genistein on Oxidative Injury in Endothelial Cells

Anti‐atherosclerotic effects of vitamin E – myth or reality?

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