补充辅酶Q10可作为肌营养不良细胞的抗氧化剂。

Cell Stress and Chaperones Pub Date : 2019-11-01 Epub Date: 2019-10-16 DOI:10.1007/s12192-019-01039-2
Daniela Sayuri Mizobuti, Aline Reis Fogaça, Fernanda Dos Santos Rapucci Moraes, Luis Henrique Rapucci Moraes, Rafael Dias Mâncio, Túlio de Almeida Hermes, Aline Barbosa Macedo, Amanda Harduim Valduga, Caroline Caramano de Lourenço, Elaine Cristina Leite Pereira, Elaine Minatel
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引用次数: 0

摘要

氧化应激增加是杜氏肌营养不良症(DMD)的一个常见特征。据报道,在肌营养不良症患者和DMD实验模型mdx小鼠中,活性氧(ROS)水平较高,与酶的抗氧化活性改变有关。在这项研究中,我们调查了辅酶Q10(CoQ10)对mdx小鼠肌营养不良症肌肉细胞原代培养物中氧化应激标记物水平和钙浓度的影响。将C57BL/10和mdx小鼠的骨骼肌细胞原代培养物用辅酶Q10(5 μM)处理24小时。MTT和活/死细胞试验表明,辅酶Q10对正常和萎缩性肌肉细胞无细胞毒性作用。mdx肌肉细胞的胞内钙浓度、H2O2生成、4-HNE和SOD-2水平较高。实验组之间的过氧化氢酶、GPx和Gr水平无明显差异。这项研究表明,CoQ10能降低氧化应激标志物(如H2O2)的水平,起到抗氧化作用,并能减少肌营养不良细胞中异常的细胞内钙离子流入。这项研究表明,辅酶Q10能降低肌肉萎缩症细胞中H2O2等氧化应激标记物的水平,起到抗氧化作用,并能减少细胞内异常钙离子流入。我们的研究结果还表明,氧化应激的减少降低了上调 SOD 和 GSH 等抗氧化途径的需要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Coenzyme Q10 supplementation acts as antioxidant on dystrophic muscle cells.

Increased oxidative stress is a frequent feature in Duchenne muscular dystrophy (DMD). High reactive oxygen species (ROS) levels, associated with altered enzyme antioxidant activity, have been reported in dystrophic patients and mdx mice, an experimental model of DMD. In this study, we investigated the effects of coenzyme Q10 (CoQ10) on oxidative stress marker levels and calcium concentration in primary cultures of dystrophic muscle cells from mdx mice. Primary cultures of skeletal muscle cells from C57BL/10 and mdx mice were treated with coenzyme Q10 (5 μM) for 24 h. The untreated mdx and C57BL/10 muscle cells were used as controls. The MTT and live/dead cell assays showed that CoQ10 presented no cytotoxic effect on normal and dystrophic muscle cells. Intracellular calcium concentration, H2O2 production, 4-HNE, and SOD-2 levels were higher in mdx muscle cells. No significant difference in the catalase, GPx, and Gr levels was found between experimental groups. This study demonstrated that CoQ10 treatment was able to reduce levels of oxidative stress markers, such as H2O2, acting as an antioxidant, as well as decreasing abnormal intracellular calcium influx in dystrophic muscles cells. This study demonstrated that CoQ10 treatment was able to reduce levels of oxidative stress markers, such as H2O2, acting as an antioxidant, as well as decreasing abnormal intracellular calcium influx in dystrophic muscles cells. Our findings also suggest that the decrease of oxidative stress reduces the need for upregulation of antioxidant pathways, such as SOD and GSH.

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