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Cytotoxicity of Malondialdehyde and Cytoprotective Effects of Taurine via Oxidative Stress and PGC-1α Signal Pathway in C2C12 Cells

机译:甘氨酸丙二醛的细胞毒性和牛磺酸的细胞保护作用=“斜体”>通过C2C12细胞中的PGC-1α信号途径和PGC-1α信号途径

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摘要

One of the end-products of ROS-induced peroxidation, malondialdehyde (MDA), induces the cross-links in proteins, which leads to perturbation of the physiological functions of cells and contributes to abnormal biological regulation and various disorders. Taurine (2-aminoethanesulfonic acid, Tau) aids in adjusting normal physiological functions to confer stress resistance. The protective effects of Tau against MDA stress in vitro or in vivo were reported previously. In this study, we had investigated the protective effects of taurine on viability, oxidative stress levels and mitochondrial biogenesis in mouse muscle C2C12 cells undergoing MDA induced stress. We show that the treatment with 100 μM MDA leads to increase in cell oxidative stress levels, inhibition of mitochondrial biogenesis and the reduction of the cell survival rates. The pretreatment with 0.1 μM taurine reduced MDA-induced death rate via inhibition of oxidative stress, restoration of mitochondrial functions of the mitochondrial membrane potential (MMP) and ATP production. In MDA stress, the pre-treatment with 0.1 μM taurine leads to upregulation of the factors of mitochondrial biogenesis. These observations suggest that the cytoprotective effects of taurine may be due to an induction of mitochondrial biogenesis.
机译:ROS诱导的过氧化的最终产物之一,丙二醛(MDA),诱导蛋白质中的交联,这导致细胞的生理功能的扰动,并有助于异常的生物调节和各种疾病。牛磺酸(2-氨基乙酰磺酸,TAU)有助于调整正常的生理功能以赋予应力性。先前报道了Tau对MDA胁迫的保护作用或体内的影响。在这项研究中,我们研究了牛磺酸对经历MDA诱导应力的小鼠肌肉C2C12细胞中的活力,氧化应激水平和线粒体生物发生的保护作用。我们表明,用100μmMDA的处理导致细胞氧化应激水平的增加,对线粒体生物发生的抑制和细胞存活率的降低。通过抑制氧化应激,恢复线粒体膜电位(MMP)和ATP生产的氧化胁迫,对MDA诱导的死亡率降低了MDA诱导的死亡率的预处理。在MDA应激中,用0.1μm牛磺酸的预处理导致对线粒体生物发生的因素的上调。这些观察结果表明,牛磺酸的细胞保护作用可能是由于线粒体生物发生的诱导。

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