核因子-κB抑制剂BAY 11-7082抑制培养血管内皮细胞内皮素-1的产生

M. Ohkita, M. Takaoka, Y. Shiota, Rumi Nojiri, M. Sugii, Y. Matsumura
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引用次数: 39

摘要

BAY 11-7082是核因子- kappab (NF-kappaB)的抑制剂,可阻止IkappaB与NF-kappaB结合的抑制蛋白磷酸化,抑制培养血管内皮细胞中基底和肿瘤坏死因子(TNF)- α诱导的内皮素(ET)-1 mRNA表达和NF-kappaB活化。BAY 11-7082显著降低内皮细胞基底和tnf α诱导的ET-1释放。这些结果表明,抑制NF-kappaB激活有助于BAY 11-7082对ET-1基因表达和ET-1释放的抑制作用,从而提示NF-kappaB在调节ET-1的产生中起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Nuclear Factor-κB Inhibitor BAY 11-7082 Suppresses Endothelin-1 Production in Cultured Vascular Endothelial Cells
BAY 11-7082, an inhibitor of nuclear factor-kappaB (NF-kappaB), which prevents a step of the phosphorylation of inhibitory protein IkappaB bound to NF-kappaB, suppressed basal and tumor necrosis factor (TNF)-alpha-induced prepro endothelin (ET)-1 mRNA expression and NF-kappaB activation in cultured vascular endothelial cells. BAY 11-7082 significantly decreased basal and TNF-alpha-induced ET-1 release from endothelial cells. These results indicate that the inhibition of NF-kappaB activation contributes to the suppressive effect of BAY 11-7082 on ET-1 gene expression and ET-1 release, thereby suggesting that NF-kappaB plays an important role in the regulation of ET-1 production.
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