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首页> 外文期刊>Cellular and molecular life sciences: CMLS >Pycnogenol inhibits tumor necrosis factor-α-induced nuclear factor kappa B activation and adhesion molecule expression in human vascular endothelial cells
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Pycnogenol inhibits tumor necrosis factor-α-induced nuclear factor kappa B activation and adhesion molecule expression in human vascular endothelial cells

机译:碧萝ogen可抑制肿瘤坏死因子-α诱导的核因子κB活化和黏附分子在人血管内皮细胞中的表达

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摘要

The transcriptional regulatory protein nuclear factor kappa B (NF-kB) participates in the control of gene expression of many modulators of inflammatory and immune responses, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). The heightened expression of these adhesion molecules has been reported to play a critical role in atherosclerosis, inflammation, ischemic vascular disorders, diabetes, and cancer metastasis. In the present study, we investigated the effect of pycnogenol, an antioxidant phytochemical, on the activation of NF-kB and the induction of VCAM-1 and ICAM-1 in tumor necrosis factor (TNF)-α-treated human umbilical vein endothelial cells (HUVECs).Gel-shift analysis of HUVEC demonstrated that pretreatment with pycnogenol exhibited a concentration-dependent suppression of TNF-α-induced activation of NF-kB. Induction of VCAM-1 and ICAM-1 surface expression by TNF-α was dose-dependently reduced by pycnogenol. TNF-α significantly increased the release of superoxide anion and hydrogen peroxide from HUVECs. Pycnogenol dose-dependently inhibited their release. The ability of pycnogenol to inhibit NF-kB activation and VCAM-1 and ICAM-1 expression suggests that this phytochemical may play an important role in halting or preventing the atherogenic process.
机译:转录调节蛋白核因子κB(NF-kB)参与多种炎症和免疫反应调节剂的基因表达控制,包括血管细胞粘附分子-1(VCAM-1)和细胞间粘附分子-1(ICAM- 1)。据报道,这些粘附分子的高表达在动脉粥样硬化,炎症,缺血性血管疾病,糖尿病和癌症转移中起关键作用。在本研究中,我们研究了抗氧化剂植物化学成分碧萝ogen对肿瘤坏死因子(α)处理的人脐静脉内皮细胞中NF-kB的活化以及VCAM-1和ICAM-1的诱导作用。 (HUVEC).HUVEC的凝胶位移分析表明,用碧容健进行预处理后,TNF-α诱导的NF-kB活化表现出浓度依赖性抑制作用。碧萝ogen可剂量依赖性地降低TNF-α诱导VCAM-1和ICAM-1表面表达。 TNF-α显着增加了HUVEC中超氧阴离子和过氧化氢的释放。碧萝ogen可剂量依赖性地抑制其释放。碧萝ogen抑制NF-kB活化以及VCAM-1和ICAM-1表达的能力表明,这种植物化学物质可能在中止或预防动脉粥样硬化过程中起重要作用。

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