Purpose

To explore genistein, the most active component of soy isoflavones, on viability, expression of estrogen receptor (ER) subtypes, choline acetyltransferase (ChAT), and glutamate receptor subunits in amyloid peptide 25-35-induced hippocampal neurons, providing valuable data and basic information for neuroprotective effect of genistein in Aβ_25-35-induced neuronal injury.

Methods

We established an in vitro model of Alzheimer's disease by exposing primary hippocampal neurons of newborn rats to amyloid peptide 25–35 (20 μM) for 24 h and observing the effects of genistein (10 μM, 3 h) on viability, expression of ER subtypes, ChAT, NMDA receptor subunit NR2B and AMPA receptor subunit GluR2 in Aβ_25-35-induced hippocampal neurons.

Results

We found that amyloid peptide 25–35 exposure reduced the viability of hippocampal neurons. Meanwhile, amyloid peptide 25–35 exposure decreased the expression of ER subtypes, ChAT and GluR2, and increased the expression of NR2B. Genistein at least partially reversed the effects of amyloid peptide 25–35 in hippocampal neurons.

Conclusion

Genistein could increase the expression of ChAT as a consequence of activating estrogen receptor subtypes, modulating the expression of NR2B and GluR2, and thereby ameliorating the status of hippocampal neurons and exerting neuroprotective effects against amyloid peptide 25–35. Our data suggest that genistein might represent a potential cell-targeted therapy which could be a promising approach to treating AD.

中文翻译：

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金雀异黄素通过调节雌激素受体，胆碱乙酰基转移酶和谷氨酸受体抑制淀粉样肽25-35诱导的神经元死亡。

目的

为了探索染料木黄酮，大豆异黄酮中最活跃的成分，对淀粉样肽25-35诱导的海马神经元的生存力，雌激素受体（ER）亚型，胆碱乙酰基转移酶（ChAT）和谷氨酸受体亚基的表达，提供了有价值的数据和基础金雀异黄素在_Aβ25-35诱导的神经元损伤中的神经保护作用的信息。

方法

我们通过将新生大鼠的原代海马神经元暴露于25–35淀粉样蛋白肽（20μM）24小时，并观察染料木黄酮（10μM，3 h）对生存力，ER亚型表达的影响，建立了阿尔茨海默氏病的体外模型，ChAT，NMDA受体亚基NR2B和AMPA受体亚基GluR2在_Aβ25-35诱导的海马神经元中。

结果

我们发现淀粉样肽25-35暴露会降低海马神经元的活力。同时，淀粉样肽25-35暴露降低了ER亚型，ChAT和GluR2的表达，并增加了NR2B的表达。金雀异黄素至少部分逆转了海马神经元中25-35淀粉样肽的作用。

结论

金雀异黄素可能通过激活雌激素受体亚型，调节NR2B和GluR2的表达而增加ChAT的表达，从而改善海马神经元的状态，并对25-35号淀粉样蛋白发挥神经保护作用。我们的数据表明，染料木黄酮可能代表一种潜在的细胞靶向疗法，这可能是治疗AD的有前途的方法。