
Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: April 22, 2025
Thlaspi arvense (TA), commonly known as "Ximi" or "Subaijiang," is a traditional Chinese medicinal herb used to prevent and treat ulcerative colitis (UC). However, the precise mechanisms underlying its therapeutic effects remain unclear, necessitating further investigation identify potential pharmaceutical applications for UC management. This study aims elucidate efficacy of TA active constituents in treatment. first evaluated varying doses on 3% dextran sulfate sodium (DSS)-induced UC. Gut microbiota alterations mice were analyzed via 16S rRNA sequencing, with correlation analyses reveal relationship between gut cytokines. Then, network pharmacology was utilized identified targets Protein-protein interaction (PPI) networks, Gene Ontology (GO), Kyoto Encyclopedia Genes Genomes (KEGG) enrichment employed explore TA's mechanisms. Molecular docking dynamics simulations validated interactions compounds UC-related targets. Finally, TNF pathway modulation by component, isovitexin, verified vitro vivo. alleviated DSS-induced weight loss dose-dependent manner, reduced disease activity indices, preserved intestinal mucosal barrier integrity. Subsequently, fluorescence situ hybridization (FISH) revealed suppressed microbial translocation tissues. To characterize inflammatory responses, ELISA demonstrated that modulated levels key cytokines (TNF-α, IL-1β, IL-6, IL-10) oxidative stress markers (SOD, MDA), indicating systemic anti-inflammatory effects. Building these findings, sequencing showed regulated alpha/beta diversity inhibited infectious disease-related pathways. Notably, heatmaps highlighted strong association TNF-α Escherichia-Shigella abundance, high-dose significantly reducing this pathogenic bacterial genus. systematically molecular mechanisms, 220 Consistent experimental data, PPI KEGG implicated TNF-α, AKT targets, primarily through signaling modulation. validate predictions, confirmed stable while specifically emphasized isovitexin's high affinity TNF-α. experiments vivo inhibition TNF-α-mediated NF-κB activation, studies isovitexin directly mitigated TNF-α-induced epithelial damage. Furthermore, potent activation tissues, constituent effectively cell damage, collectively highlighting their complementary Collectively, (TA) ameliorates synergistic involving modulation, suppression, preservation. By remodeling communities reduce colonization translocation. concurrently inhibits TNF-α/NF-κB-driven inflammation, regulation. attenuates demonstrating multi-scale efficacy. These findings establish multi-target spanning host-microbe intracellular signaling, providing rationale standardizing TA-based formulations advancing precision agent bowel diseases.
Language: Английский