Abstract：
Alzheimer\'s disease (AD) is a neurodegenerative brain disorder that progressively impairs long-term and working memory. The function and mechanism of PA(Patchouli alcohol) in improving AD in the external treatment of encephalopathy remain unclear. This study aimed to investigate the therapeutic effect of PA on AD using an Aβ1-42 induced AD mouse model with LPS(Lipopolysaccharide) stimulation of BV2 microglial cells. Additionally, we aimed to explore the potential mechanism of PA in enhancing autophagy and reducing neuroinflammation through the AMPK (AMP-activated protein kinase)/mTOR (Mammaliam target of rapamycin) signaling pathway. The Morris water maze was used to assess cognitive function, and cortical and hippocampal tissues were collected for further analysis of the corresponding signaling pathways and inflammatory changes through biological experiments. Our research findings demonstrate that PA has a significant positive impact on cognitive and memory impairments in mice that have been induced with Aβ1-42-induced AD. Additionally, PA was also found to revert the activation of microglia induced by LPS. These effects may be attributed to the reduction of neuroinflammation and enhancement of the AMPK/mTOR autophagy pathway. Therefore, PA may serve as an effective therapeutic option to prevent or delay the progression of AD-associated memory dysfunction.
摘要：
阿尔茨海默病（AD）是一种神经退行性脑疾病，可逐渐损害长期和工作记忆。广滞性醇(PA)在脑病外用治疗中改善AD的作用及机制尚不清楚。本研究旨在通过LPS（脂多糖）刺激BV2小胶质细胞的Aβ1-42诱导的AD小鼠模型，探讨PA对AD的治疗作用。此外,我们旨在探讨PA通过AMPK(AMP活化蛋白激酶)/mTOR(哺乳动物雷帕霉素靶蛋白)信号通路增强自噬和减轻神经炎症的潜在机制。莫里斯水迷宫用于评估认知功能，收集皮质和海马组织,通过生物学实验进一步分析相应的信号通路和炎症变化。我们的研究结果表明，PA对Aβ1-42诱导的AD诱导的小鼠的认知和记忆障碍具有显著的积极影响。此外,还发现PA逆转LPS诱导的小胶质细胞的活化。这些作用可能归因于神经炎症的减少和AMPK/mTOR自噬途径的增强。因此,PA可以作为预防或延缓AD相关记忆功能障碍进展的有效治疗选择。
