Elucidating the Action Mechanism of Shenling Baizhu Powder in the Treatment of Ulcerative Colitis Based on Network Pharmacology andExperimental Validation

Objective: To elucidate the therapeutic mechanisms of Shenling Baizhu Powder (SLBZ) in treating ulcerative colitis (UC) through an integrated approach combining network pharmacology and experimental validation, highlighting its potential as an alternative or complementary therapy. Methods: The active constituents and corresponding targets of SLBZ were identified using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). UC-related targets were obtained from DrugBank and the Comparative Toxicogenomics Database (CTD). Overlapping targets were visualized using a Venn diagram, and protein- protein interactions were mapped using the STRING database. The "compound-componentdisease- target" network was constructed through GO function analysis and KEGG pathway enrichment analysis. Molecular docking was performed using Discovery Studio 4.5 software. A UC mouse model was induced with dextran sodium sulfate (DSS), and mice were divided into normal, UC, SLBZ (low, medium, high doses), and mesalazine groups, treated for 14 days. Histopathological changes in colon tissues were assessed, and serum levels of IL-4, TNF-α, and HIF-1α were measured by immunohistochemistry to verify SLBZ';s targets in UC treatment. Results: A total of 408 active ingredients and 2118 corresponding targets were identified in SLBZ, with 2052 targets associated with UC, resulting in 610 overlapping targets. Further refinement identified 54 active ingredients and 86 targets, with quercetin, betulin, catharanthamine, and glyasperin B as key components. Core targets included TP53, AKT1, JUN, and HSP90AA1. KEGG analysis suggested SLBZ';s involvement in PI3K/Akt, JAK2/STAT3, and TNF signaling pathways. Molecular docking confirmed strong binding affinities between key targets and main components. Histological analysis showed that SLBZ alleviated DSS-induced colonic tissue injury, while immunohistochemistry revealed reduced expression of TNF-α and STAT3, and upregulated IL-4, indicating modulation of the JAK/STAT3 pathway. Conclusion: SLBZ exerts therapeutic effects on UC by targeting key proteins (e.g., TP53, AKT1, JUN) and modulating critical pathways (e.g., JAK2/STAT3). This study provides a theoretical basis for the potential of SLBZ as a multi-targeted therapeutic agent for UC, which can be further explored through clinical trials and multi-omics analyses to validate its efficacy and safety.