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C3-富勒烯-三-甲烷二羧酸可保护小脑颗粒细胞免于凋亡。

C3-fullero-tris-methanodicarboxylic acid protects cerebellar granule cells from apoptosis.

作者信息

Bisaglia M, Natalini B, Pellicciari R, Straface E, Malorni W, Monti D, Franceschi C, Schettini G

机构信息

Institute of Chemistry and Technology of Drugs, University of Perugia, Italy.

出版信息

J Neurochem. 2000 Mar;74(3):1197-204. doi: 10.1046/j.1471-4159.2000.741197.x.

DOI:10.1046/j.1471-4159.2000.741197.x
PMID:10693952
Abstract

Buckminsterfullerenols were recently investigated for their protective properties in different models of acute and chronic neurodegeneration. We tested C3-fullero-tris-methanodicarboxylic acid in our in vitro model of apoptotic neuronal death, which consists of shifting the culture K+ concentration from 25 to 5 mM for rat cerebellar granule cells. The impairment of mitochondrial respiratory function as well as chromatin derangement and fragmentation of DNA in apoptotic oligonucleosomes that occur in these conditions were protected by this compound in a concentration-dependent way. To assess whether antioxidant activity could account for the rescue of cerebellar granule cells from apoptosis, we tested the fullerene derivative under FeSO4-induced oxidative stress and found significant protection. Thus, we visualized membrane and cytoplasmic peroxides and reactive oxygen species and found a significant reduction of the species after 24 h in 5 mM K+ with the fullerene derivative. Such evidence suggests that this compound exerts a protective role in cerebellar granule cell apoptosis, likely reducing the oxidative stress.

摘要

最近对巴克敏斯特富勒烯醇在急性和慢性神经退行性变的不同模型中的保护特性进行了研究。我们在凋亡神经元死亡的体外模型中测试了C3-富勒烯-三-甲烷二羧酸,该模型是将大鼠小脑颗粒细胞的培养钾离子浓度从25 mM转变为5 mM。在这些条件下发生的凋亡寡核小体中线粒体呼吸功能的损害以及染色质紊乱和DNA片段化,都受到该化合物浓度依赖性的保护。为了评估抗氧化活性是否可以解释小脑颗粒细胞从凋亡中获救,我们在硫酸亚铁诱导的氧化应激下测试了富勒烯衍生物,发现有显著的保护作用。因此,我们观察了膜和细胞质中的过氧化物以及活性氧,发现在含有富勒烯衍生物的5 mM钾离子环境中24小时后这些物质显著减少。这些证据表明,该化合物在小脑颗粒细胞凋亡中发挥保护作用,可能是通过减轻氧化应激来实现的。

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