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Taurine Chloramine Activates Nrf2 Increases HO-1 Expression and Protects Cells from Death Caused by Hydrogen Peroxide

机译:牛磺酸氯胺激活Nrf2增加HO-1表达并保护细胞免于过氧化氢导致的死亡

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摘要

Hypochlorous acid (HOCl) is toxic and causes cell death. However, this effect is inhibited by reaction with taurine, which generates taurine chloramine (TauCl), thereby protecting the cells from HOCl-generated toxicity. TauCl has been shown to inhibit the production of inflammatory mediators like O2•−, H2O2 and NO. In this study, RAW 264.7 macrophages treated with TauCl were protected from death caused by H2O2. TauCl increased the expression of peroxiredoxin-1, thioredoxin-1 and heme oxygenase (HO)-1, the anti-oxidant enzymes normally induced by activation of NF-E2-related factor-2 (Nrf2). TauCl increased nuclear translocation of Nrf2 and binding to the anti-oxidant response element. These data suggest that TauCl produced abundantly in the activated neutrophils and released to surrounding cells in the inflamed tissues may induce the expression of cytoprotective anti-oxidant enzymes. Elevation of HO activity via induction of HO-1 expression within neighboring cells may provide protection from cytotoxicity caused by inflammatory oxidants like H2O2.
机译:次氯酸(HOCl)有毒,可导致细胞死亡。但是,与牛磺酸反应会抑制该作用,牛磺酸会生成牛磺酸氯胺(TauCl),从而保护细胞免受HOCl产生的毒性的影响。已显示TauCl抑制炎症介质的产生,例如O2 •-,H2O2和NO。在这项研究中,用TauCl处理的RAW 264.7巨噬细胞受到保护,免受H2O2引起的死亡。 TauCl增加了过氧化物酶1,硫氧还蛋白1和血红素加氧酶(HO)-1的表达,血红素加氧酶(HO)-1是通常由激活NF-E2相关因子2(Nrf2)诱导的抗氧化剂。 TauC1增加了Nrf2的核易位并与抗氧化反应元件结合。这些数据表明,TauC1在活化的中性粒细胞中大量产生并释放到发炎组织中的周围细胞中,可能诱导细胞保护性抗氧化酶的表达。通过诱导邻近细胞内HO-1表达诱导HO活性的升高可提供针对由诸如H 2 O 2的炎性氧化剂引起的细胞毒性的保护。

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