Alzheimer's disease (AD) is one of the most serious neurodegenerative diseases and is characterized by progressive cognitive impairment and multiple neurological changes. To date, there are no effective drugs to delay or cure AD. Breviscapine (Bre) is an active ingredient of flavonoids extracted from breviscapus. Previous research suggests that Bre is an effective medicine for the prevention and treatment of AD. In the present study, we sought to explore the molecular mechanisms responsible for short-term beneficial effects of Breviscapine on Aβ burden, neuronal and synaptic, cognitive function in APP/PS1 transgenic mice at 6 months age. Our results showed that 3 months of intraperitoneal treatment with Bre rescued learning deficits, relieved memory retention, improved the ability to explore the outside world, markedly decreased Aβ burden, attenuated function of neocortical and hippocampal neuron, and increased the synaptic proteins levels in the brain of APP/PS1 mice by decreasing BACE1, promoting Aβ-degrading enzyme IDE expression, suppressing RAGE expression, and regulating p38/p53/NT4 pathway. This finding provides more evidence of neuroprotective effects and action mechanisms of Bre antagonist AD, suggesting that Bre may have potential as anti-AD agent.

中文翻译：

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灯盏花素通过APP / PS1转基因小鼠的多种机制发挥神经保护作用。

阿尔茨海默氏病（AD）是最严重的神经退行性疾病之一，其特征是进行性认知障碍和多种神经系统变化。迄今为止，还没有有效的药物可以延缓或治愈AD。灯盏花素（Bre）是从灯盏花中提取的类黄酮的活性成分。先前的研究表明，Bre是预防和治疗AD的有效药物。在本研究中，我们寻求探索负责灯盏花素对6个月大的APP / PS1转基因小鼠的Aβ负荷，神经元和突触，认知功能的短期有益作用的分子机制。我们的结果表明，Bre腹膜内治疗3个月可挽救学习缺陷，减轻记忆力，改善探索外界的能力，显着降低Aβ负担，通过减少BACE1，促进Aβ降解酶IDE表达，抑制RAGE表达和调节p38 / p53 / NT4通路，减弱了新皮层和海马神经元的功能，并增加了APP / PS1小鼠大脑中的突触蛋白水平。这一发现为Bre拮抗剂AD的神经保护作用和作用机制提供了更多证据，表明Bre可能具有作为抗AD剂的潜力。