Abstract：Objective：To explore the mechanisms of prevention and treatment of Alzheimer's Disease (AD) by Dihuang Yinzi using network pharmacology combined with experimental verification. Methods：All chemical components of Dihuang Yinzi were obtained by TCMSP and HERB databases， and the eligible active components were screened based on the pharmacokinetic information of chemical components and literature search， and the corresponding predicted targets were further obtained by TCMSP， SwissTargetPrediction and STITCH databases. AD- related targets were collected using the Therapeutic Target Database，GeneCards and DisGeNET database. Cytoscape 3.7.1 software was used to construct the "herb- component- target" network. The Metascape web tool was used to analyze the targets for GO and KEGG pathway enrichment. The mouse model of AD was constructed by scopolamine. Y- maze， new object recognition and Morris water maze were used to evaluate the learning and memory ability of the mice. The levels of acetylcholinesterase (AChE)，tumor necrosis factor-α(TNF-α)，interleukin-6 (IL-6) in the hippocampus were detected by ELISA. The expressions of nuclear factor (NF-κB) and phospho-NF-κB (p- NF- κB) in the hippocampus were detected by Western Blot. Results： A total of 61 key active components in Dihuang Yinzi were screened by central network topology analysis， and 106 key targets were identified in AD. GO enrichment analysis revealed that key targets were involved in peptide binding (amyloid)，acetylcholine binding，neurotransmitter receptor activity，regulation of inflammatory response， behavior， etc. KEGG pathway enrichment analysis revealed that AChE， CHRNA7， RELA， and TNF and other key targets were enriched in cholinergic synapses， NF- κB signaling pathway. In vivo experiments showed that Dihuang Yinzi pretreatment improved the cognitive function of AD mice，inhibited the levels of AChE，IL-6 and TNF-α，and inhibited the expression levels of p-NF- κB proteins. Conclusion：Dihuang Yinzi may reduce cholinergic damage by inhibiting the level of AChE in the mouse hippocampus， further inhibiting NF- κB- mediated neuroinflammation and restoring the "cholinergic anti- inflammatory pathway"， thus improve the cognitive dysfunction in mice and preventing AD.