Abstract
BACKGROUND: Yiyi Fuzi Baijiang powder (YFB), a classic Chinese medicine, significantly affects ulcerative colitis (UC). However, it remains unclear whether YFB plays a therapeutic role by improving the intestinal flora of UC patients and its active ingredients. AIM: To explore the mechanisms of action of YFB in treating UC. METHODS: A mouse model of UC was established by drinking 2.5% dextran sulfate sodium (DSS). Mice were treated with YFB. 16S rDNA sequencing was used to detect changes in intestinal flora and perform functional predictions. Corresponding target genes of core active ingredients in YFB and UC were obtained using multiple database retrievals and then used to predict the mechanism of overlapping targets. After screening core ingredients and target genes, AutoDock software was used for molecular docking, and the best binding target was selected to verify binding activity. RESULTS: YFB improved DSS-UC mice by restoring body weight, reducing disease activity index, increasing water and food intake, and alleviating diarrhea and local histopathological damage. YFB enhanced beta diversity, decreased pathogenic bacteria such as Turicibacter and Clostridium_sensu_stricto_1, and increased probiotics such as unclassified_f_Lachnospiraceae and Akkermansia. However, it also reduced anaerobic probiotics such as Ruminococcus, Enterorhabdus and Bifidobacterium. Network pharmacology identified 17 pathways, with cancer and adipocytokine signaling pathways showing significant differences in predicting intestinal microbial function. Molecular docking revealed that nuclear factor kappa-B inhibitor A, RELA and NFKB1, and colchamine, morusin and orotinin had docking scores > 5.0. CONCLUSION: YFB treats UC by reducing harmful bacteria and boosting probiotics to restore intestinal balance, while potentially influencing signaling pathways.