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当代阿耳茨海默病研究

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Research Article

假蒟通过抑制SH-SY5Y细胞中的淀粉样蛋白形成和Tau蛋白过磷酸化来减少β -淀粉样蛋白(Aβ)诱导的神经毒性

卷 18, 期 1, 2021

发表于: 24 March, 2021

页: [80 - 87] 页: 8

弟呕挨: 10.2174/1567205018666210324124239

价格: $65

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摘要

背景：在阿尔茨海默病中，β淀粉样蛋白(Aβ)的积累触发淀粉样蛋白的形成和 Tau蛋白的过度磷酸化导致神经元细胞死亡。假蒟（PS）是马来人常用的一种传统草药，用于治疗风湿、头痛和增强记忆力。它具有抗胆碱能、抗炎、抗氧化、抗抑郁等多种生物学作用。 目的：本研究旨在探讨PS对Aβ诱导的神经毒性的保护作用，并探讨其潜在的作用机制。 方法：研究了PS叶(L)和根(R)的正己烷(HXN)、二氯甲烷(DCM)、乙酸乙酯(EA)和甲醇(MEOH)提取物对Aβ诱导的人神经母细胞瘤细胞的神经保护作用。PS预处理24 h后，Aβ诱导24 h。采用细胞活力和细胞活性氧(ROS)测定方法研究了PS的神经保护作用。测定细胞外Aβ和Tau蛋白的苏氨酸231 (pT231)磷酸化水平。分别使用qRT-PCR和western blot分析基因和蛋白表达。 结果：PS (LHXN和RHXN)的己烷提取物可以保护SH-SY5Y细胞免受Aβ诱导的神经毒性，并降低细胞外Aβ和磷酸化Tau蛋白(pT231)的水平。虽然PS的提取物抑制β全身的活性氧产量,但不太可能具有神经保护效应，只是由于PS进一步的抗氧化能力,机械性的研究表明PS的神经保护作用可能是由于其通过下调BACE和APP来调节淀粉样生成的能力。 结论：这些发现表明，PS的己烷提取物通过减少淀粉样蛋白的形成和Tau蛋白的过度磷酸化，对SH-SY5Y细胞的Aβ诱导的神经毒性具有神经保护作用。由于其神经保护功能，PS可能是一种潜在的治疗阿尔茨海默病的药物。

关键词: 假蒟，阿尔兹海默症，β-淀粉样蛋白，Tau过度磷酸化，淀粉样蛋白形成，神经保护

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