Inhibition of THP-1 cell adhesion to endothelial cells by α-tocopherol and α-tocotrienol is dependent on intracellular concentration of the antioxidants

Noguchi, Noriko; Hanyu, Ryuhei; Nonaka, Aya; Okimoto, Yuko; Kodama, Tatsuhiko

doi:10.1016/s0891-5849(03)00216-8

Cited by 82 publications

(54 citation statements)

References 31 publications

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“…4). These results suggest that reduction of monocyte adhesion by tocotrienol is attributed to decreased adhesion molecule expresinhibitory action on monocytic cell adherence when Recently, Noguchi et al [8] clearly gave reason for the differences among these tocotrienols in inhibitory effects on monocyte-endothelial interaction.…”

Section: Inhibition Of Cholesterol Synthesis By Tocotrienolmentioning

confidence: 85%

“…OxLDL can induce endothelial dysfunction (2) and expression of cytokines (3), growth factors, and several cell surface adhesion molecules (4) that are capable of recruiting circulating monocytes and T lymphocytes into the intima. OxLDL activates the development of monocytes into macrophages where the uptake of oxLDL via the scavenger receptor is rapid (5,6), and inhibits the migration of macrophages (8). OxLDL stimulates cell proliferation and transmigration of smooth muscle cells (7).…”

Section: Oxidized Ldl Hypothesismentioning

confidence: 99%

“…It has been demonstrated that tocotrienol has a potent action for inhibition of lipid peroxidation [6], inhibition of monocyte adherence [7,8], and neuroprotection [9] compared with tocopherol. This review focuses on recent advances that have revealed the mechanisms by which tocotrienol may exert its protection against atherosclerosis.…”

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confidence: 99%

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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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Section: Inhibition Of Cholesterol Synthesis By Tocotrienolmentioning

confidence: 85%

Section: Oxidized Ldl Hypothesismentioning

confidence: 99%

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Tocotrienols and Atherosclerosis

Naito

Shimozawa

Yoshikawa

2004

J. Clin. Biochem. Nutr.

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“…Genes Nutr (2012) 7:75-81 79 accumulates in endothelial cells to levels that are 30-50 fold greater compared with alpha-tocopherol (Naito et al 2005;Noguchi et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms underlying the radioprotective properties of γ-tocotrienol: comparative gene expression profiling in tocol-treated endothelial cells

Berbée

Boerma

et al. 2011

Genes Nutr

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Among the eight naturally occurring vitamin E analogs, c-tocotrienol (GT3) is a particularly potent radioprophylactic agent in vivo. Moreover, GT3 protects endothelial cells from radiation injury not only by virtue of its antioxidant properties but also by inhibition of 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase and by improving the availability of the nitric oxide synthase cofactor tetrahydrobiopterin. Nevertheless, the precise mechanisms underlying the superior radioprotective properties of GT3 compared with other tocols are not known. This study, therefore, examined the differences in gene expression profiles between GT3 and its tocopherol counterpart, c-tocopherol, as well as between GT3 and a-tocopherol in human endothelial cells. Cells were treated with vehicle or the appropriate tocol for 24 h, after which total RNA was isolated and genome-wide gene expression profiles were obtained using the Illumina platform. GT3 was far more potent in inducing gene-expression changes than a-tocopherol or c-tocopherol. In particular, GT3 induced multiple changes in pathways known to be of importance in the cellular response to radiation exposure. Affected GO functional clusters included response to oxidative stress, response to DNA damage stimuli, cell cycle phase, regulation of cell death, regulation of cell proliferation, hematopoiesis, and blood vessel development. These results form the basis for further studies to determine the exact importance of differentially affected GO functional clusters in endothelial radioprotection by GT3.

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“…Relative to a-tocotrienol, c-tocotrienol displayed 1.5-fold more profound inhibitory effect on monocytic cell adherence using a 15-lM concentration within 24 h. This inhibitory action was reversed by coincubation with farnesol and geranylgeraniol, suggesting a role for prenylated proteins in the regulation of monocyte adhesion. The increased intracellular accumulation of a-tocotrienol when compared to a-tocopherol may also play a role in the higher potency of a-tocotrienol to inhibit the adhesiveness of endothelial cells (Noguchi et al 2003). Among the isoforms of tocotrienols, d-tocotrienols showed to exhibit a highest inhibitory action on monocytic cell adherence (Naito et al 2005).…”

Section: Monocytic Adhesion Property Of Tocotrienol In Cardioprotectionmentioning

confidence: 99%

Multifaceted role of tocotrienols in cardioprotection supports their structure: function relation

2011

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Tocotrienols are a class of vitamin E which modulates several mechanisms associated with cardioprotection, anti-cancer, anti-diabetic, and neuroprotection. Unlike other Vitamin E-like compounds, tocotrienols possess inimitable properties. Quite a lot of studies have determined the cardioprotective abilities of tocotrienols and have been shown to possess novel hypocholesterolemic effects together with an ability to reduce the atherogenic apolipoprotein and lipoprotein plasma levels. In addition, tocotrienol has been suggested to have an antioxidant, anti-thrombotic, and antitumor effect indicating that tocotrienol may serve as an effective agent in the prevention and/or treatment of cardiovascular disease and cancer. The bioactivity exhibited is due to the structural characteristics of tocotrienols. Rich sources of tocotrienols which include rice bran, palm oil, and other edible oils exhibit protective effect against cardiovascular disorders. The conclusions drawn from the early literature that vitamin E group of compounds provides an inevitable role in cardioprotection is sustained in many more recent studies.

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Inhibition of THP-1 cell adhesion to endothelial cells by α-tocopherol and α-tocotrienol is dependent on intracellular concentration of the antioxidants

Cited by 82 publications

References 31 publications

Tocotrienols and Atherosclerosis

Tocotrienols and Atherosclerosis

Mechanisms underlying the radioprotective properties of γ-tocotrienol: comparative gene expression profiling in tocol-treated endothelial cells

Multifaceted role of tocotrienols in cardioprotection supports their structure: function relation

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