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首页> 外文期刊>Brain research >Neuroprotection of inositol hexaphosphate and changes of mitochondrion mediated apoptotic pathway and alpha-synuclein aggregation in 6-OHDA induced parkinson's disease cell model
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Neuroprotection of inositol hexaphosphate and changes of mitochondrion mediated apoptotic pathway and alpha-synuclein aggregation in 6-OHDA induced parkinson's disease cell model

机译：6-OHDA诱发帕金森病细胞模型中六磷酸肌醇的神经保护作用和线粒体介导的凋亡途径和α-突触核蛋白聚集的变化

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Animal and cell experiments showed that inositol hexaphosphate (IP6) was protective on neurons in parkinson's disease (PD) model, but the underlying mechanism of this action was not extensively elucidated. To address this question, we established 6-hydroxydopamine (6-OHDA) induced human dopaminergic cell line SH-SY5Y as PD cell model and testified the neuroprotection of IP6. Through hoechst nuclear stain method and flow cytometric analysis, apoptosis induced by 6-OHDA was blocked by IP6 pretreatment. Significant protection against reactive oxygen species (ROS) and lipid peroxidation product malondialdehyde (MDA) was observed in 6-OHDA induced cells pretreated with IP6. To further investigate the mechanism of anti-apoptotic effect of IP6, expression of mediators in mitochondrion dependent apoptotic pathway was detected. Results indicated that loss of mitochondrial membrane potential, cytochrome c releasing, upregulation of Bcl-2-associated X protein (Bax), downregulation of B-cell CLL/lymphoma 2 (Bcl-2) and caspases activation were reversed by IP6. In addition, using flow cytometric method and western blot approach, our data showed that IP6 attenuated the rise of calcium and alpha-synuclein aggregation in cytosol. Collectively, IP6 exerted its neuroprotection on dopaminergic cells in PD cell model and the mechanism may be associated with changes of mitochondrion mediated apoptotic pathway and a-synuclein aggregation. (c) 2015 Elsevier B.V. All rights reserved.
机译：动物和细胞实验表明，肌醇六磷酸（IP6）对帕金森氏病（PD）模型中的神经元具有保护作用，但尚未广泛阐明这种作用的潜在机制。为了解决这个问题，我们建立了6-羟基多巴胺（6-OHDA）诱导的人多巴胺能细胞系SH-SY5Y作为PD细胞模型，并证明了IP6的神经保护作用。通过hoechst核染色法和流式细胞仪分析，IP6预处理可阻断6-OHDA诱导的细胞凋亡。在用IP6预处理的6-OHDA诱导的细胞中观察到对活性氧（ROS）和脂质过氧化产物丙二醛（MDA）的显着保护作用。为了进一步研究IP6的抗凋亡作用机理，检测了线粒体依赖性凋亡途径中介导因子的表达。结果表明，IP6可逆转线粒体膜电位的丧失，细胞色素c的释放，Bcl-2相关X蛋白（Bax）的上调，B细胞CLL /淋巴瘤2（Bcl-2）的下调和胱天蛋白酶的激活。此外，使用流式细胞仪和蛋白质印迹法，我们的数据显示IP6减弱了细胞溶质中钙和α-突触核蛋白聚集的上升。总的来说，IP6在PD细胞模型中对多巴胺能细胞发挥了神经保护作用，其机制可能与线粒体介导的凋亡途径的改变和α-突触核蛋白的聚集有关。 （c）2015 Elsevier B.V.保留所有权利。

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