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首页> 外文期刊>The European Journal of Neuroscience >Galantamine protects against oxidative stress induced by amyloid-beta peptide in cortical neurons.
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Galantamine protects against oxidative stress induced by amyloid-beta peptide in cortical neurons.

机译：加兰他敏可防止由皮质神经元中的淀粉样β肽诱导的氧化应激。

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摘要

Galantamine is currently used in the treatment of patients with mild-to-moderate Alzheimer's disease (AD). Although its action is mostly directed at the regulation of cholinergic transmission, galantamine can also afford neuroprotection against amyloid-beta peptide (Abeta), which is involved in AD pathogenesis. In this study, we used cultured rat cortical neurons treated with two forms of Abeta(1-40), fresh and previously aged (enriched in fibrils). First, we confirmed that galantamine prevented neurodegeneration induced by both peptide forms in a concentration-dependent manner. Moreover, we observed that when neurons were co-incubated with fresh Abeta(1-40) plus galantamine, the amount of amyloid aggregates was reduced. As oxidative conditions influence Abeta aggregation, we investigated whether galantamine prevents oxidative stress induced by this peptide. The data show that either fresh or aged Abeta(1-40) significantly increased the amount of reactive oxygen species and lipoperoxidation, these effects being prevented by galantamine. In Abeta(1-40)-treated neurons, the depletion of reduced glutathione (GSH) seems to be related to the decrease in glutathione peroxidase and glutathione reductase activities(.) These alterations in the GSH antioxidant system were prevented by galantamine. Overall, these results constitute the first evidence that galantamine can prevent the neuronal oxidative damage induced by Abeta, providing an in vitro basis for the beneficial actions of galantamine in the AD neurodegenerative process.
机译：加兰他敏目前用于治疗轻度至中度阿尔茨海默氏病（AD）的患者。尽管它的作用主要针对胆碱能传递的调节，但加兰他敏还可以提供针对AD发病机理的淀粉样β肽（Abeta）的神经保护作用。在这项研究中，我们使用培养的大鼠皮质神经元，分别用新鲜和预先老化（富含原纤维）的两种形式的Abeta（1-40）处理。首先，我们证实加兰他敏以浓度依赖的方式阻止了两种肽形式诱导的神经变性。此外，我们观察到将神经元与新鲜Abeta（1-40）和加兰他敏共同孵育时，淀粉样蛋白聚集体的数量减少了。由于氧化条件影响Abeta聚集，我们研究了加兰他敏是否能阻止该肽诱导的氧化应激。数据显示，新鲜的或陈旧的Abeta（1-40）均显着增加了活性氧和脂过氧化的量，而加兰他敏可以阻止这些作用。在Abeta（1-40）处理的神经元中，减少的谷胱甘肽（GSH）的消耗似乎与谷胱甘肽过氧化物酶和谷胱甘肽还原酶活性的降低有关。总的来说，这些结果构成了加兰他敏可以预防Abeta诱导的神经元氧化损伤的第一个证据，为加兰他敏在AD神经变性过程中的有益作用提供了体外基础。

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