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首页> 外文期刊>The Journal of Nutritional Biochemistry >Sulforaphane reduces vascular inflammation in mice and prevents TNF-alpha-induced monocyte adhesion to primary endothelial cells through interfering with the NF-kappa B pathway
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Sulforaphane reduces vascular inflammation in mice and prevents TNF-alpha-induced monocyte adhesion to primary endothelial cells through interfering with the NF-kappa B pathway

机译：萝卜硫烷可减轻小鼠的血管炎症，并通过干扰NF-κB通路防止TNF-α诱导的单核细胞粘附于原代内皮细胞

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Sulforaphane, a naturally occurring isothiocyanate present in cruciferous vegetables, has received wide attention for its potential to improve vascular function in vitro. However, its effect in vivo and the molecular mechanism of sulforaphane at physiological concentrations remain unclear. Here, we report that a sulforaphane concentration as low as 0.5 mu M significantly inhibited tumor necrosis factor-alpha (TNF-alpha)-induced adhesion of monocytes to human umbilical vein endothelial cells, a key event in the pathogenesis of atherosclerosis both in static and under flow conditions. Such physiological concentrations of sulforaphane also significantly suppressed TNF-alpha-induced production of monocyte chemotactic protein-1 and adhesion molecules including soluble vascular adhesion molecule-1 and soluble E-selectin, key mediators in the regulation of enhanced endothelial cell-monocyte interaction. Furthermore, sulforaphane inhibited TNF-alpha-induced nuclear factor (NF)-kappa B transcriptional activity, Inhibitor of NF-kappa B alpha (I kappa B alpha) degradation and subsequent NF-kappa B p65 nuclear translocation in endothelial cells, suggesting that sulforaphane can inhibit inflammation by suppressing NF-kappa B signaling. In an animal study, sulforaphane (300 ppm) in a mouse diet significantly abolished TNF-alpha-increased ex vivo monocyte adhesion and circulating adhesion molecules and chemokines in C57BL/6 mice. Histology showed that sulforaphane treatment significantly prevented the eruption of endothelial lining in the intima layer of the aorta and preserved elastin fibers' delicate organization, as shown by Verhoeff-van Gieson staining. Immunohistochemistry studies showed that sulforaphane treatment also reduced vascular adhesion molecule-1 and monocyte-derived F4/80-positive macrophages in the aorta of TNF-alpha-treated mice. In conclusion, sulforaphane at physiological concentrations protects against TNF-alpha-induced vascular endothelial inflammation, in both in vitro and in vivo models. This anti-inflammatory effect of sulforaphane may be, at least in part, associated with interfering with the NF-kappa B pathway. (C) 2014 Elsevier Inc. All rights reserved.
机译：萝卜硫素是十字花科蔬菜中天然存在的异硫氰酸盐，因其在体外改善血管功能的潜力而受到广泛关注。然而，其在体内的作用以及在生理浓度下萝卜硫烷的分子机制仍不清楚。在这里，我们报告说，萝卜硫烷浓度低至0.5μM会显着抑制肿瘤坏死因子-α（TNF-alpha）诱导的单核细胞与人脐静脉内皮细胞的粘附，这是动脉粥样硬化发病机理的关键事件在流动条件下。这样的生理浓度的萝卜硫烷还显着抑制了TNF-α诱导的单核细胞趋化蛋白1的产生以及包括可溶性血管黏附分子1和可溶性E-选择素在内的黏附分子，这是调节内皮细胞-单核细胞相互作用的关键介体。此外，萝卜硫烷抑制内皮细胞中TNF-α诱导的核因子（NF）-κB的转录活性，NF-κBα（IκBα）降解的抑制剂和随后的NF-κBp65核易位，这表明萝卜硫烷可以通过抑制NF-κB信号传导来抑制炎症。在一项动物研究中，小鼠饮食中的萝卜硫素（300 ppm）显着消除了C57BL / 6小鼠中TNF-α增加的离体单核细胞粘附以及循环粘附分子和趋化因子。组织学表明，萝卜硫烷处理可显着阻止主动脉内膜层内皮层的喷发，并保留弹性蛋白纤维的细腻组织，如Verhoeff-van Gieson染色所示。免疫组织化学研究表明，萝卜硫烷处理还可以降低TNF-α处理的小鼠主动脉中的血管粘附分子1和单核细胞衍生的F4 / 80阳性巨噬细胞。总之，在体外和体内模型中，处于生理浓度的萝卜硫素都可以抵抗TNF-α诱导的血管内皮炎症。萝卜硫烷的这种抗炎作用可能至少部分与干扰NF-κB途径有关。 （C）2014 Elsevier Inc.保留所有权利。

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