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- W3141526250 abstract "动脉粥样硬化是长期的煽动性的疾病。像使用费的受体(TLR4 ) 4 是重要发信号受体并且在煽动性的反应起一个关键作用。Poly (自动数据处理核糖)(PARP1 ) 聚合酶 1 是能调整各种各样的煽动性的基因的表示的原子酶。在这研究,我们调查了角色, lipopolysaccharide (LPS ) 上的 PARP1 的内在的机制在人的大动脉的 endothelial 房间导致了发炎。与控制相比, LPS 刺激增加了 TLR4 和 PARP1 的蛋白质表达式。TLR4 抑制象 PARP1 一样减少了可诱导的氮的氧化物 synthase (iNOS ) 和 ICAM-1 的导致 LPS 的 upregulation。原子因素 B (NF-B ) 抑制减少了 ICAM-1 和 iNOS 表示。PARP1 的抑制减少了煽动性的 cytokines 的蛋白质表示由 LPS 刺激导致了,可能通过阻止 NF-B 原子 translocation。我们的学习证明 LPS 经由 TLR4/PARP1/NF-B 小径增加了 ICAM-1 和 iNOS 表示。PARP1 可能是在在 LPS 刺激以后的调停 TLR4 的发炎的一个不可缺少的因素。PARP1 抑制可能在动脉粥样硬化期间使导致 LPS 的煽动性的 cytokines 表示的处理清楚些。" @default.
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- W3141526250 date "2012-01-01" @default.
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- W3141526250 title "Poly(ADP-ribose) polymerase 1 inhibition protects human aortic endothelial cells against LPS-induced inflammation response" @default.
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