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首页> 外文期刊>Food & Function >DHA and vitamin E antagonized the A beta 25-35-mediated neuron oxidative damage through activation of Nrf2 signaling pathways and regulation of CD36, SRB1 and FABP5 expression in PC12 cells+
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DHA and vitamin E antagonized the A beta 25-35-mediated neuron oxidative damage through activation of Nrf2 signaling pathways and regulation of CD36, SRB1 and FABP5 expression in PC12 cells+

机译：DHA和维生素E对β25-35介导的神经元氧化损伤，通过激活NRF2信号传导途径和CD36，SRB1和FABP5表达中的CD36，SRB1和FABP5表达+

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摘要

The present study was designed to explore the neuroprotective effects of docosahexaenoic acid (DHA) and/or vitamin E (VE) in vitro. The PC12 cells were pretreated with DHA and/or VE for 4 h, followed by 50 mol L-1 A(25-35) treatments for another 48 h. The cells were then collected and used for the measurements of oxidative stress parameters. Real time-PCR and western blot were applied to measure fatty acid transporters, Nrf2 and its downstream antioxidant targets' gene and protein expression. Our results indicated that the A(25-35) treatment inhibited cellular growth, increased intracellular ROS generation and decreased the mitochondrial membrane potential. The A(25-35) treatment decreased the total antioxidant capacity (T-AOC), whereas it increased the MDA levels in neuron cells. Pretreatment of cells with VE or DHA could antagonize the A(25-35)-mediated cell growth inhibition and mitochondrial membrane potential decline. Activation of the Nrf2 signaling pathway and regulation of CD36, SRB1 and FABP5 expression were observed in DHA- and DHA + VE-pretreated cells. Our results indicated a synergistic effect of DHA and VE in antagonizing the oxidative damage caused by A(25-35) in the PC12 cells. The results of the present study will shed light on the application of nutritional intervention for DHA and VE in preventing neuronal damage-related diseases.
机译：本研究旨在探讨二十二碳六烯酸（DHA）和/或维生素E（VE）体外的神经保护作用。用DHA和/或VE预处理PC12细胞4小时，然后再适用50 mol L-1 A（25-35）处理48小时。然后收集细胞并用于测量氧化应激参数。施用实时PCR和Western印迹以测量脂肪酸转运蛋白，NRF2及其下游抗氧化靶的基因和蛋白质表达。我们的结果表明，A（25-35）治疗抑制细胞生长，增加细胞内ROS产生并降低线粒体膜电位。 A（25-35）处理降低了总抗氧化能力（T-AOC），而它增加了神经元细胞中的MDA水平。使用VE或DHA的细胞预处理可以拮抗A（25-35）介导的细胞生长抑制和线粒体膜潜在下降。在DHA和DHA + VE预处理细胞中观察到NRF2信号传导途径和CD36，SRB1和FABP5表达的调节。我们的结果表明DHA和VE在PC12细胞中由（25-35）引起的氧化损伤进行了协同作用。本研究的结果将阐明营养干预对DHA和VE预防神经元损伤相关疾病的应用。

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  • 来源
    《Food & Function》 |2019年第2期|共13页
  • 作者

    Huang Xiaochen; Zhen Jie; Dong Shengqi; Zhang Huiqiang; Van Halm-Lutterodt Nicholas; Yuan Linhong;

  • 作者单位

    Capital Med Univ Sch Publ Hlth Beijing 100069 Peoples R China;

    Capital Med Univ Sch Publ Hlth Beijing 100069 Peoples R China;

    Capital Med Univ Sch Publ Hlth Beijing 100069 Peoples R China;

    Capital Med Univ Sch Publ Hlth Beijing 100069 Peoples R China;

    Capital Med Univ Beijing Tiantan Hosp Dept Neurosurg Beijing 100050 Peoples R China;

    Capital Med Univ Sch Publ Hlth Beijing 100069 Peoples R China;

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  • 正文语种 eng
  • 中图分类 食品工业;
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