Komatsuna Seed Extracts Protection Against Amyloid β(1-42)-Induced Neuronal Cell Death
Komatsuna Seed Extracts Protection Against Amyloid β(1-42)-Induced Neuronal Cell Death
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DOI：
10.4172/2155-6156.1000368
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发表时间：
2014-05
期刊：
影响因子：
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通讯作者：
Y. Okada;M. Okada
中科院分区：
文献类型：
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作者：
Y. Okada;M. Okada
目的：阿尔茨海默病（AD）作为“3型糖尿病”受到关注，并且很明显，这种神经退行性疾病与糖尿病具有多种共同的病理。进行性痴呆，脑中淀粉样β（Aβ）蛋白沉积增加是AD的标志。Aβ导致Aβ相关的活性氧（ROS）产生和细胞死亡。本研究探讨了小松种子提取物（KSE）对Aβ（1-42）诱导的海马神经元（HN）神经毒性和细胞死亡过程的调节作用。方法：选择16种植物。采用SDS凝胶电泳技术研究了植物种子水提物（PSAE）对Aβ结构的修饰作用。用CCK-8法测定细胞活力，评价KSE的神经保护作用。此外，我们还进行了KSE的抗糖基化实验和抗聚集实验，以进一步证实KSE的修饰机制。为了发现KSE对Aβ诱导的氧化应激的影响，我们使用2 '，7'-二氯荧光素二乙酸酯测定法检测了KSE。为了进一步阐明KSE对Aβ诱导的细胞死亡的影响，我们检测了KSE对葡萄糖摄取的影响。结果：小松菜、菜豆和青更菜中均未检测到Aβ蛋白。KSE显示出增加细胞存活，相当于100%阻断Aβ诱导的细胞死亡。KSE可降低BSA和乳清蛋白的糖基化水平。此外，当细胞用KSE处理时，由Aβ处理引起的细胞内ROS积累减少。KSE改善HN中Aβ对葡萄糖的摄取。结论：KSE抑制Aβ诱导的细胞死亡。KSE通过修饰Aβ降低Aβ的毒性。KSE改善Aβ葡萄糖摄取的抑制，从而修饰Aβ。KSE抑制Aβ产生的细胞内ROS。这些结果表明KSE保护细胞的可能性。
Objective: Alzheimer’s disease (AD) is receiving attention as “Type 3 diabetes” and it is evident that this neurodegenerative disease has multiple shared pathologies with diabetes mellitus. Progressive dementia, increased deposition of amyloid β (Aβ) protein in the brain is the hallmark of AD. Aβ leads to Aβ associated Reactive Oxygen Species (ROS) production and cell death. In this study, we investigated the effects of Komatsuna Seed Extracts (KSE) on Aβ (1-42)-induced neurotoxicity and on the regulation of cell death processing in hippocampus neurons (HN). Methods: We selected sixteen plants. We investigated the effects of plant seeds’ aqueous extractson (PSAE) on Aβ structure modification using SDS gel electrophoresis. The neuroprotective effects of KSE were evaluated by measuring the cell viability with a CCK-8 assay. Furthermore, we carried out an anti-glycation experiment of KSE and an anti-aggregation experiment of KSE to confirm the modification mechanism of KSE. To find the effects of KSE on Aβ-induced oxidative stress, we examined KSE using a 2’, 7’-dichlorofluorescein diacetate assay. To further unravel the effects of KSE on Aβ-induced cell death, we examined the influence of KSE on glucose uptake. Results: No bands of Aβ were recognized in Komatsuna, Common bean or Qing gengcai. KSE showed enhancement of cell survival amounting to a 100% blockade of Aβ-induced cell death. KSE caused the decrease in BSA and lactalbumin glycation. Furthermore, intracellular ROS accumulation resulting from Aβ treatment was reduced when cells were treated with KSE. KSE improves glucose uptake by Aβ in HN. Conclusion: KSE inhibits Aβ-induced cell death. KSE reduces the toxicity of Aβ by modifying Aβ. KSE improves the inhibition of Aβ glucose uptake thereby modifying Aβ. KSE inhibits ROS in cells produced by Aβ. The possibility that KSE protects cells was suggested by these results.