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首页> 外文期刊>Mycotoxin Research >Fumonisin B-1-induced oxidative stress triggers Nrf2-mediated antioxidant response in human hepatocellular carcinoma (HepG2) cells
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Fumonisin B-1-induced oxidative stress triggers Nrf2-mediated antioxidant response in human hepatocellular carcinoma (HepG2) cells

机译：Fumonisin B-1诱导的氧化应激触发人肝细胞癌（HepG2）细胞中的NRF2介导的抗氧化反应

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Fumonisin B-1 (FB1), a causative agent for animal-related mycotoxicoses, has been implicated in human and animal cancer. FB1 induces oxidative stress but the related survival responses are not well established. Central to this response is the transcription factor, nuclear factor erythroid 2 p45-related factor 2 (Nrf2). The effects of FB1 on Nrf2-related survival responses in human hepatoma (HepG2) cells were investigated. HepG2 cells were treated with 200mol/l FB1 (IC50-24h). Cellular redox status was assessed via the quantification of intracellular reactive oxygen species (ROS), lipid peroxidation, protein oxidation and the antioxidant glutathione (GSH). The protein expression of oxidative stress and mitochondrial stress response proteins [Nrf2, phosphorylated-Nrf2 (pNrf2), superoxide dismutase 2 (SOD2), catalase (CAT), sirtuin 3 (Sirt 3) and Lon-protease 1 (Lon-P1)] were quantified by western blotting, while gene expression levels of SOD2, CAT and GPx were assessed using quantitative polymerase chain reaction (qPCR). Lastly, the fluorometric, JC-1 assay was used to determine mitochondrial polarisation. FB1 significantly increased ROS (p0.001), and induced lipid peroxidation (p&0.05) and protein carbonylation (p0.001), which corresponded with the increase in GSH levels (p&0.05). A significant increase in pNrf2, SOD2, SOD2, CAT (p&0.05), CAT (p0.01) and GPx (p0.001) expression was observed; however, total Nrf2 (p&0.05) was reduced. There was also a minor reduction in the mitochondrial membrane potential of HepG2 cells (p&0.05); however, the expression of Sirt 3 and Lon-P1 (p0.001) were upregulated. Exposure to FB1 induced oxidative stress in HepG2 cells and initiated Nrf2-regulated transcription of antioxidants.
机译：Fumonisin B-1（FB1），一种动物相关霉菌毒素的致病剂，涉及人和动物癌症。 FB1诱导氧化应激，但相关的存活反应不是很好的。对该响应的核心是转录因子，核因子红细胞2 P45相关因子2（NRF2）。研究了FB1对人肝癌（HepG2）细胞NRF2相关存活反应的影响。用200mol / L FB1（IC50-24H）处理HepG2细胞。通过细胞内反应性氧（ROS），脂质过氧化，蛋白质氧化和抗氧化剂谷胱甘肽（GSH）的定量评估细胞氧化还原状态。氧化应激和线粒体应激响应蛋白的蛋白质表达[NRF2，磷酸化-NRF2（PNRF2），超氧化物歧化酶2（SOD2），过氧化氢酶（猫），Sirtuin 3（Sirt 3）和Lon-Protease 1（Lon-P1）]通过Western印迹量化，而使用定量聚合酶链反应（QPCR）评估SOD2，CAT和GPX的基因表达水平。最后，荧光测定的JC-1测定法用于确定线粒体极化。 FB1显着增加了ROS（P0.001），并诱导脂质过氧化（P＆amp; 0.05）和蛋白质羰基化（P0.001），其与GSH水平的增加相对应（P＆amp; 0.05）。观察到PNRF2，SOD2，SOD2，猫（P＆amp; 0.05），猫（P0.01）和GPX（P0.001）表达的显着增加;但是，降低了总NRF2（P＆amp; 0.05）。 HepG2细胞的线粒体膜电位也略有降低（P＆amp; 0.05）;然而，上调SIRT 3和LON-P1（P0.001）的表达。暴露于HepG2细胞中的FB1诱导的氧化应激并引发NRF2调节的抗氧化转录。

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