Astragalin improves cognitive disorder in Alzheimer's disease: Based on network pharmacology and molecular docking simulation.
Rui DuHongyan PeiZhongmei HeJin WangXiaohong ZhouWenyan LiDiwei ZhuCaiqun ZhangPublished in: CNS neuroscience & therapeutics (2024)
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.
Keyphrases
- molecular docking
- lipopolysaccharide induced
- lps induced
- molecular dynamics simulations
- traumatic brain injury
- inflammatory response
- cognitive impairment
- oxidative stress
- cognitive decline
- poor prognosis
- induced apoptosis
- stem cells
- gene expression
- high fat diet induced
- type diabetes
- spinal cord injury
- neuropathic pain
- bone marrow
- cerebral ischemia
- adipose tissue
- insulin resistance
- single cell
- working memory
- mild cognitive impairment
- signaling pathway
- mesenchymal stem cells
- brain injury
- subarachnoid hemorrhage
- combination therapy