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首页> 外文期刊>Toxicological sciences: An official journal of the Society of Toxicology >Modulation of serum growth factor signal transduction in Hepa 1-6 cells by acetaminophen: an inhibition of c-myc expression, NF-kappaB activation, and Raf-1 kinase activity.
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Modulation of serum growth factor signal transduction in Hepa 1-6 cells by acetaminophen: an inhibition of c-myc expression, NF-kappaB activation, and Raf-1 kinase activity.

机译：对乙酰氨基酚对Hepa 1-6细胞中血清生长因子信号转导的调节：对c-myc表达，NF-κB活化和Raf-1激酶活性的抑制。

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摘要

Acetaminophen (APAP) is a widely used analgesic and antipyretic that can lead to severe liver damage when taken at excessive doses. APAP toxicity results when cytochrome P450-generated APAP metabolites trigger an oxidative stress and covalently modify target proteins. APAP has also been reported to inhibit cells from completing S-phase through a cytochrome P450-independent mechanism, raising the possibility that APAP may directly suppress liver regeneration and repair. Here we show that APAP also inhibits entrance of Hepa 1-6 cells into the cell cycle by blocking a number of events associated with the G0-G1 transition. We have found that APAP inhibits serum growth factor activation of c-myc expression, NF-kappaB DNA binding, and Raf kinase. Therefore, the ability of APAP to inhibit passage of cells through both G1 and S phases might interfere with organ regeneration and thus exacerbate acute liver damage caused by APAP.
机译：对乙酰氨基酚（APAP）是一种广泛使用的止痛药和退热药，过量服用会导致严重的肝脏损害。当细胞色素P450产生的APAP代谢产物触发氧化应激并共价修饰靶蛋白时，会导致APAP毒性。据报道，APAP还可以通过不依赖细胞色素P450的机制抑制细胞完成S期，从而增加了APAP直接抑制肝再生和修复的可能性。在这里，我们显示APAP还可以通过阻止与G0-G1过渡相关的许多事件来抑制Hepa 1-6细胞进入细胞周期。我们发现，APAP抑制血清生长因子激活c-myc表达，NF-kappaB DNA结合和Raf激酶。因此，APAP抑制细胞通过G1期和S期的能力可能会干扰器官再生，从而加剧APAP引起的急性肝损伤。

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