血管细胞活化、功能和凋亡的调节:抗氧化剂和核因子κ B的作用。

C Weber, W Erl
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引用次数: 33

摘要

nf - κ B的活性与内皮细胞的炎症激活及其粘附性密切相关,并且似乎通过协调抗凋亡程序来调节SMC中的凋亡。NF-kappa B的活性已在人动脉粥样硬化或血管成形术后被发现,但在未病变的动脉中未被发现。因此,如本文所述,抗氧化剂或抗炎剂或腺病毒I κ B α过表达抑制nf - κ B动员可能协同抑制内皮细胞活化并诱导SMC凋亡。这种协同概念可能是一种血管保护方法,通过减轻新生和进展中的动脉粥样硬化病变的炎症反应和SMC增殖,以及血管成形术后形成的新内膜形成,来预防动脉粥样硬化和再狭窄。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Modulation of vascular cell activation, function, and apoptosis: role of antioxidants and nuclear factor-kappa B.

The activity of NF-kappa B is critically involved in the inflammatory activation of endothelial cells and their adhesiveness and also appears to regulate apoptosis in SMC by coordinating antiapoptotic programs. The activity of NF-kappa B has been revealed within human atheromas or following angioplasty but not in undiseased arteries. Hence, the inhibition of NF-kappa B mobilization by antioxidative or anti-inflammatory agents or by adenoviral I kappa B alpha overexpression, as reviewed herein, may act in concert to suppress endothelial activation and to induce SMC apoptosis. This synergistic concept may be a vasoprotective approach to prevent atherogenesis and restenosis by attenuating inflammatory reactions and SMC proliferation in nascent and progressing atherosclerotic lesions, as well as in developing neointima formations following angioplasty.

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