Induction of the Nrf2-driven antioxidant response by tert-butylhydroquinone prevents ethanol-induced apoptosis in cranial neural crest cells.
Induction of the Nrf2-driven antioxidant response by tert-butylhydroquinone prevents ethanol-induced apoptosis in cranial neural crest cells.
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DOI：
10.1016/j.bcp.2010.03.004
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发表时间：
2010-07-01
影响因子：
5.8
通讯作者：
Chen, Shao-yu
中科院分区：
文献类型：
--
作者：
Yan, Dong;Dong, Jian;Sulik, Kathleen K.;Chen, Shao-yu
先前的研究表明，酒精暴露会导致脑神经脊细胞(NCCs)凋亡，NCCs是一种与胎儿酒精谱系障碍(FASD)有关的酒精敏感细胞群。此外，通过激活核因子-红系2相关因子2(NRF2)诱导内源性抗氧化剂，已被证明可以防止乙醇暴露的小鼠胚胎的氧化应激和细胞凋亡。本研究的目的是检测Nrf2诱导剂叔丁基对苯二酚(TBHQ)是否能保护NCCs免受乙醇诱导的细胞凋亡。乙醇暴露可引起NCCs中Nrf2及其下游抗氧化剂蛋白表达的适度增加。单独用TBHQ处理NCCs后，Nrf2及其下游抗氧化剂的蛋白表达显著增加，抗氧化酶活性也显著提高。在暴露在乙醇中的NCC中，TBHQ介导的抗氧化反应阻止了氧化应激和细胞凋亡。这些结果清楚地表明，Nrf2信号的激活对乙醇诱导的NCCs的凋亡具有保护作用。
Previous studies have shown that ethanol exposure causes apoptosis in cranial neural crest cells (NCCs), an ethanol-sensitive cell population implicated in Fetal Alcohol Spectrum Disorders (FASD). Additionally, induction of endogenous antioxidants through activation of nuclear factor-erythroid 2-related factor 2 (Nrf2) has been shown to prevent oxidative stress and apoptosis in ethanol-exposed mouse embryos. The objective of this study was to test whether tert-butylhydroquinone (tBHQ), an Nrf2 inducer, can protect NCCs against ethanol-induced apoptosis. Ethanol exposure was shown to cause a moderate increase in the protein expression of Nrf2 and its downstream antioxidants in the NCCs. Treatment of NCCs with tBHQ alone significantly increased the protein expression of Nrf2 and its downstream antioxidants and also significantly increased the activities of the antioxidant enzymes. In NCCs exposed to ethanol, the tBHQ-mediated antioxidant response prevented oxidative stress and apoptosis. These results clearly demonstrate that activation of Nrf2 signaling confers protection against ethanol-induced apoptosis in NCCs.
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