College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, China.
The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
CNS Neurosci Ther. 2024 Aug;30(8):e14799. doi: 10.1111/cns.14799.
We investigate the mechanism of action of astragalin (AST) in the treatment of Alzheimer's disease (AD). Network pharmacology was conducted to analyze the relationships among AST, AD, and neuroinflammation, The APP/PS1 transgenic mice with AD were used in the experiments; to be specific, the influence of AST on the behavior of mice was analyzed by Morris water maze and eight-arm radial maze tests, the tissue inflammatory factor levels were detected by ELISA, and pathological changes were analyzed by H&E and immunohistochemical staining. Analysis results of network pharmacology suggested that AST exerted the multi-target effect on neuroinflammation in AD. Through molecular docking and dynamics analyses, COX2 might be the target of AST. Moreover, animal experimental results demonstrated that AST improved the behavior of AD mice, and enhanced the motor and memory abilities, meanwhile, it suppressed the expression of inflammatory factors in tissues and the activation of microglial cells. this study discovers that AST can suppress microglial cell activation via COX2 to improve neuroinflammation in AD.
我们研究了毛蕊异黄酮（AST）在治疗阿尔茨海默病（AD）中的作用机制。通过网络药理学分析 AST、AD 和神经炎症之间的关系，在 APP/PS1 转基因 AD 小鼠中进行实验；具体来说，通过 Morris 水迷宫和八臂放射迷宫测试分析 AST 对小鼠行为的影响，通过 ELISA 检测组织炎性因子水平，通过 H&E 和免疫组织化学染色分析病理变化。网络药理学分析结果表明，AST 对 AD 中的神经炎症发挥了多靶点作用。通过分子对接和动力学分析，COX2 可能是 AST 的靶点。此外，动物实验结果表明，AST 改善了 AD 小鼠的行为，增强了运动和记忆能力，同时抑制了组织中炎症因子的表达和小胶质细胞的激活。本研究发现，AST 可以通过 COX2 抑制小胶质细胞的激活，改善 AD 中的神经炎症。
