Objective This research is intended to assess the influence of Yinzhihuang (YZH) in Alcohol-associated Liver Disease and explore its potential mechanisms in alcohol-induced liver injury in mice using network pharmacology. Methods A chronic alcoholic liver disease mouse model was constructed in 4- to 6-week-old male C57BL/6 mice using the Lieber-DeCarli diet feeding method. The mice were randomly divided into three groups: (1) the control group (Pair-fed); (2) the alcohol group (EtOH-fed); (3) the YZH treatment group (EtOH-fed+YZH). The control group was fed a calorie-matched control diet daily, the alcohol group was fed a diet containing 5% (v/v) ethanol daily, and the YZH treatment group was administered YZH (0.5 mL/kg) daily in addition to the ethanol diet. Liver injury was evaluated through serum ALT and AST levels and histological analysis, while changes in mRNA levels of lipid metabolism, synthesis, and inflammatory factors were measured using qRT-PCR. Components are collected and targets are predicted via the TCMSP database, while ALD disease targets are retrieved from TTD, OMIM, and DRUGBANK databases. Subsequently, the intersection is obtained using Venny2.1.0. The protein-protein interaction (PPI) network is constructed using the STRING database, and the intersecting targets are subjected to GO function and KEGG pathway enrichment analysis via the Metascape database. Results Compared with the control group, the levels of AST and TG in the alcohol group of mice were increased, and the mRNA levels of TNF-α, IL-1β, and SREBP-1c were elevated. Meanwhile, the mRNA level of PPAR-α was decreased, and the protein levels of TNF-α and F4/80 were increased. The YZH treatment group significantly reduced the serum AST levels in mice after alcohol consumption (P<0.05), alleviated alcohol-induced lipid accumulation, and significantly decreased serum TG levels. It also markedly reduced immune cell infiltration and liver inflammation at both the mRNA and protein levels. Pharmacological network analysis revealed 75 active components in YZH, among which quercetin and aloin may be the primary active components. These components may act on 95 targets related to Alcohol-associated Liver Disease (ALD), including tumor necrosis factor (TNF), interleukin-6 (IL-6), albumin (ALB), interleukin-1β (IL-1β), and prostaglandin-endoperoxide synthase 2 (PTGS2), which are key targets involved in the pathological process of ALD. The primary biological processes involved include transcriptional regulation, lipid homeostasis, and DNA damage-induced apoptosis. KEGG enrichment analysis suggests that the regulation of ALD by YZH may involve key pathways such as the PI3K/Akt signaling pathway. Conclusion YZH has been shown to effectively improve alcohol-induced hepatic injury, lipid accumulation, and inflammatory responses. This efficacy is attributed to its key active components, such as quercetin and aloin, which target multiple sites and participate in the regulation of multiple pathways. These components exert therapeutic effects on alcoholic liver disease (ALD) through anti-inflammatory and anti-oxidative stress pathways.