Mechanism Analysis of Fuzheng Xiaokui Formula in Treating RecurrentAphthous Ulcers Based on Network Pharmacology

Introduction: Recurrent Aphthous Ulcers (RAU), the most common oral mucosal disorder, represent a chronic inflammatory condition that significantly impacts patients’ quality of life. Fuzheng Xiaokui Formula (FZXKF), an empirical prescription derived from veteran traditional Chinese medicine practitioners, has demonstrated remarkable clinical efficacy in preliminary applications. This study aimed to systematically identify the potential anti-RAU active components of FZXKF and elucidate their underlying mechanisms. Methods: Public databases were utilized to identify the primary functional ingredients and targets of FZXKF and RAU-related genes. The herb-ingredient-target and protein-protein interaction (PPI) networks were constructed and analyzed using Cytoscape 3.10.3 to identify active ingredients and core targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to identify relevant biological mechanisms and signaling pathways. Molecular docking was performed to validate interactions between key components and targets. Results: A total of 105 active components and 829 potential targets were preliminarily screened from FZXKF. Cross-referencing these with 2,903 RAU-related targets yielded 397 common targets. The 20 main active ingredients identified included glaucoside,c_qt, baicalein, isoflavanone, isorhamnetin, peonidin, etc. PPI network analysis identified 10 core targets (e.g., SRC, PIK3R1, PIK3CA, STAT3). Enrichment analysis revealed that the biological processes primarily involved responses to xenobiotic stimulus, protein phosphorylation, and oxidative stress, with significant enrichment in the PI3K-Akt, MAPK, Ras, and Rap1 signaling pathways. Molecular docking results showed strong binding affinity of primary bioactive ingredients toward core targets. Conclusion: This study successfully predicted the multi-component, multi-target, and multi-pathway mechanisms of FZXKF in treating RAU and provided a basis for further investigation into its molecular mechanisms.