Objective: In this study, the gastric injury model of rats induced by anhydrous ethanol was used to verify the gastric protective effect of special dietary Hewei peptide, and the related pathway targets were screened by network pharmacology, which provided experimental basis for clinical application. Methods: Male SD rats were selected for preventive administration, and different doses of Hewei peptide and positive drug ranitidine were given respectively. After the administration, except for the normal control group, anhydrous ethanol was used to establish the model for 1 h. Abdominal aortic blood was collected and gastric tissue was taken. The morphological characteristics of gastric wall were observed by naked eye and HE and PAS staining, and the expression of interleukin-6 ( IL-6 ) and catalase ( CAT ) in serum was detected. The chemical constituents of each drug in Hewei peptide were obtained from TCMSP and HERB databases, and Venn diagram was drawn by searching for relevant targets in GeneCards and OMIM databases. PPI network diagram was drawn by STRING website, Cytoscape3.9.1 software and DAVID platform, and GO and KEGG enrichment analysis was carried out. CytoScape 3.9.1 software was used to construct the drug-active component-disease-target network diagram of Hewei peptide, and to predict the core targets and main active components of Hewei peptide for gastric protection. Results: The results of physiological and biochemical indexes and HE and PAS staining in animal experiments showed that special diet and Weitai peptide had protective effects on acute gastric injury induced by anhydrous ethanol in rats. The results of network pharmacology showed that Hewei peptide may play a role in preventing gastric injury by acting on core targets such as TP53, EGFR and AKT1, and regulating inflammatory signals such as PI3K-Akt and MAPK. Conclusion: Hewei peptide plays a role in preventing gastric injury by regulating the level of inflammatory factors, reducing oxidative stress, maintaining the integrity of gastric mucus barrier, and regulating PI3K-Akt, MAPK and other inflammatory signaling pathways.