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[丙二醛对C2C12细胞的细胞毒性及牛磺酸通过氧化应激和PGC-1α信号通路的细胞保护作用]

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

作者信息

Cai J-G, Luo L-M, Tang H, Zhou L

机构信息

School of Sports, Hunan University of Science and Technology, Xiangtan city, Hunan province, 411201 China.

Hunan Electrical College of Technology, Xiangtan city, Hunan province, 411203 China.

出版信息

Mol Biol (Mosk). 2018 Jul-Aug;52(4):616-627. doi: 10.1134/S0026898418040043.

Abstract

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.

摘要

活性氧诱导的过氧化反应的终产物之一,丙二醛(MDA),会诱导蛋白质发生交联,从而导致细胞生理功能紊乱,并促成异常的生物调节和各种疾病。牛磺酸(2-氨基乙磺酸,Tau)有助于调节正常生理功能以赋予抗应激能力。先前已有报道称牛磺酸在体外或体内对MDA应激具有保护作用。在本研究中,我们调查了牛磺酸对遭受MDA诱导应激的小鼠肌肉C2C12细胞的活力、氧化应激水平和线粒体生物发生的保护作用。我们发现,用100μM MDA处理会导致细胞氧化应激水平升高、线粒体生物发生受到抑制以及细胞存活率降低。用0.1μM牛磺酸预处理可通过抑制氧化应激、恢复线粒体膜电位(MMP)和ATP产生的线粒体功能来降低MDA诱导的死亡率。在MDA应激中,用0.1μM牛磺酸预处理会导致线粒体生物发生因子上调。这些观察结果表明,牛磺酸的细胞保护作用可能归因于线粒体生物发生的诱导。

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