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首页> 外文期刊>The Journal of toxicological sciences >Reduction of arsenic-induced cytotoxicity through Nrf2/HO-1 signaling in HepG2 cells

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Reduction of arsenic-induced cytotoxicity through Nrf2/HO-1 signaling in HepG2 cells

机译：通过Nrf2 / HO-1信号降低HepG2细胞中砷诱导的细胞毒性

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Our previous study indicated that Nrf2 is a key transcription factor in cellular defenses against inorganic arsenite (iAsIII). However, the role of heme oxygenase-1 (HO-1), which is regulated by Nrf2, in iAsIII-induced cytotoxicity is poorly understood. To address this issue, we examined the contribution of HO-1 to iAsIII-mediated Nrf2 activation and in protection against iAsIII cytotoxicity in HepG2 cells. Exposure of HepG2 cells to iAsIII (10 μM) caused persistent induction of HO-1 accompanied by prolonged Nrf2 activation, whereas siRNA-mediated knockdown of HO-1 decreased prolonged Nrf2 activation. Pretreatment with either HO-1 siRNA or HO inhibitor (tin protoporphyrin IX) significantly enhanced iAsIII-induced cytotoxicity. These results suggest that iAsIII-induced HO-1 appears, at least in part, to act as a positive feedback regulator of Nrf2 activation, thereby diminishing its cytotoxicity in HepG2 cells.

机译：我们先前的研究表明Nrf2是细胞防御无机亚砷（iAsIII）的关键转录因子。但是，人们对由Nrf2调节的血红素加氧酶-1（HO-1）在iAsIII诱导的细胞毒性中的作用了解得很少。为了解决此问题，我们检查了HO-1对iAsIII介导的Nrf2活化的作用以及在保护HepG2细胞中对抗iAsIII细胞毒性的作用。 HepG2细胞暴露于iAsIII（10μM）会导致HO-1的持续诱导，并伴有Nrf2的延长活化，而siRNA介导的HO-1的敲低降低了Nrf2的延长活化。用HO-1 siRNA或HO抑制剂（锡原卟啉IX）进行预处理可显着增强iAsIII诱导的细胞毒性。这些结果表明，iAsIII诱导的HO-1似乎至少部分充当Nrf2激活的正反馈调节剂，从而降低其在HepG2细胞中的细胞毒性。

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《The Journal of toxicological sciences》 |2010年第3期|共5页
作者
Yumi Abiko; Yasuhiro Shinkai; Daigo Sumi; Yoshito Kumagai;
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中图分类药学;
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