Notoginsenoside R1 attenuates amyloid-β-induced damage in neurons by inhibiting reactive oxygen species and modulating MAPK activation
Notoginsenoside R1 attenuates amyloid-β-induced damage in neurons by inhibiting reactive oxygen species and modulating MAPK activation
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DOI：
10.1016/j.intimp.2014.06.018
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发表时间：
2014-09-01
影响因子：
5.6
通讯作者：
Sun, Xiaobo
中科院分区：
文献类型：
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作者：
Ma, Bo;Meng, Xiangbao;Sun, Xiaobo
淀粉样蛋白-β（A β）的进行性积累是阿尔茨海默病（AD）的病理标志。A β增加神经元细胞中自由基的产生，导致氧化应激和细胞死亡。通过减少自由基减少A β相关神经毒性的干预可以促进AD的治疗。三七皂苷R1（NR1）是中药三七中最主要和最有效的成分，可以减少活性氧，具有一定的神经保护作用。在这里，NR1被应用于基于细胞的阿尔茨海默病模型。在与A β（25 - 35）孵育的培养的PC12神经元细胞中评估细胞活力、细胞死亡、活性氧物质产生和线粒体膜电位。在该模型中，A β具有神经毒性并诱导坏死和凋亡;然而，NR1通过增加细胞活力、减少氧化损伤（包括凋亡）、恢复线粒体膜电位和抑制应激激活的MAPK信号通路显著抵消了A β的作用。这些结果有望成为治疗阿尔茨海默病和其他A β病理学相关的神经退行性疾病的潜在药物。(C)2014爱思唯尔有限公司版权所有。
Progressive accumulation of amyloid-beta (A beta) is a pathological hallmark of Alzheimer's disease (AD). A beta increases free radical production in neuronal cells, leading to oxidative stress and cell death. An intervention that would reduce A beta-related neurotoxicity through free radical reduction could advance the treatment of AD. Notoginsenoside R1 (NR1), the major and most active ingredient in the herb Panax notoginseng, can reduce reactive oxygen species and confer some neuroprotective effects. Here, NR1 was applied in a cell-based model of Alzheimer's disease. Cell viability, cell death, reactive oxygen species generation, and mitochondrial membrane potential were assessed in cultured PC12 neuronal cells incubated with A beta(25-35). In this model, A beta was neurotoxic and induced necrosis and apoptosis; however, NR1 significantly counteracted the effects of A beta by increasing cell viability, reducing oxidative damage (including apoptosis), restoring mitochondrial membrane potential, and suppressing stress-activated MAPK signaling pathways. These results promise a great potential agent for Alzheimer's disease and other A beta pathology-related neuronal degenerative disease. (C) 2014 Elsevier B.V. All rights reserved.