海藻糖(而非其他糖类)能保护 HT22 细胞免受淀粉样蛋白-β 的毒性侵害

Yue Xu , Kartar Singh , Michael A. Beazely , Zoya Leonenko
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摘要

海藻糖作为阿尔茨海默病的健康补充剂,由于其神经保护潜力,被认为主要是由于其通过代谢途径调节病理性淀粉样蛋白(a β)的产生和聚集。然而,海藻糖对神经元系统抗淀粉样蛋白毒性的影响尚不清楚。本研究通过研究不同浓度海藻糖对HT22细胞活力的影响,探讨海藻糖是否能直接降低外源性a β1 - 42寡聚物引起的细胞死亡。我们使用MTT细胞活力测定来评估HT22细胞单独暴露于外源性Aβ1-42寡聚物或与海藻糖和其他几种糖联合暴露于外源性Aβ1-42寡聚物的活力。我们的研究结果表明,海藻糖对a β1 - 42低聚物的细胞活力有保护作用,而其他糖,乳果糖、蔗糖和果糖,对淀粉样蛋白毒性没有保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Trehalose, but not other sugars, protects HT22 cells against amyloid-beta toxicity
Trehalose sugar is being explored as a health supplement in Alzheimer’s Disease due to its neuroprotective potential, which is hypothesized to be mainly due to its regulation of pathological amyloid-beta (Aβ) production and aggregation via metabolic pathways. However, the impact of trehalose on neuronal systems against amyloid toxicity is unclear. This work presents a study of the impact of trehalose at different concentrations on HT22 cell viability and explores whether trehalose can directly reduce cell death caused by exogenous Aβ1–42 oligomers. We used an MTT cell viability assay to evaluate the viability of HT22 cells exposure to exogenous Aβ1–42 oligomers alone or in combination with trehalose and several other sugars. Our results reveal that trehalose has a protective effect on the cell viability against Aβ1–42 oligomers, while other sugars, lactulose, sucrose, and fructose, provided no protection against amyloid toxicity.
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