神经炎症
安普克
自噬
PI3K/AKT/mTOR通路
小胶质细胞
莫里斯水上航行任务
医学
神经科学
信号转导
海马结构
药理学
炎症
蛋白激酶A
化学
生物
细胞生物学
激酶
内科学
细胞凋亡
生物化学
作者
Li-Ting Lin,Shuting Zhang,Bing Shang,Yi Dai,Xiaoqing Cheng,Qingguang Wu,Ruoting Zhan,Sijun Liu
标识
DOI:10.1016/j.brainresbull.2024.111030
摘要
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.
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