Abstract
Silymarin is known to have an anti-atherosclerotic activity, but the mechanism responsible for it remains unclear. Here, we demonstrate a possible mechanism involved in the anti-atherosclerotic activity of silymarin. Silymarin inhibited THP-1 cell adhesion to human umbilical vein endothelial cells (HUVECs). Silymarin also suppressed the TNF-alpha-induced protein and mRNA expression of adhesion molecules, such as VCAM-1, ICAM-1 and E-selectin, in HUVECs. Moreover, silymarin suppressed the TNF-alpha-induced DNA binding of NF-kappaB/Rel in HUVECs. Taken together, these results demonstrate that silymarin exerts an anti-atherosclerotic activity, at least in part, by inhibiting the expression of adhesion molecules.
MeSH terms
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Cell Adhesion / drug effects
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Cell Adhesion / genetics
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Cell Adhesion Molecules / biosynthesis
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Cell Adhesion Molecules / drug effects
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Cell Adhesion Molecules / genetics*
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Cell Membrane / drug effects
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Cell Membrane / metabolism
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Cells, Cultured
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DNA / metabolism
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E-Selectin / drug effects
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E-Selectin / genetics
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E-Selectin / metabolism
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Endothelium, Vascular / cytology
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Endothelium, Vascular / drug effects*
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Gene Expression / drug effects
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Humans
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Intercellular Adhesion Molecule-1 / drug effects
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Intercellular Adhesion Molecule-1 / genetics
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Intercellular Adhesion Molecule-1 / metabolism
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Monocytes / cytology
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Monocytes / drug effects
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NF-kappa B / drug effects
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NF-kappa B / metabolism
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Silymarin / pharmacology*
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Tumor Necrosis Factor-alpha / pharmacology*
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Umbilical Veins / cytology
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Umbilical Veins / drug effects*
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Vascular Cell Adhesion Molecule-1 / drug effects
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Vascular Cell Adhesion Molecule-1 / genetics
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Vascular Cell Adhesion Molecule-1 / metabolism
Substances
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Cell Adhesion Molecules
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E-Selectin
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NF-kappa B
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Silymarin
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Tumor Necrosis Factor-alpha
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Vascular Cell Adhesion Molecule-1
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Intercellular Adhesion Molecule-1
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DNA