Xiao Yang, Song Xu, Ying Tong, Jichu Luo, Xixing Fang, Jiaxing Du, Changyuan Zhou, Guangnian Hu, Bao Yang, Qisong Zhang
These effects were weakened in PGF mice but reproduced by FMT from LBTE-treated donors, confirming microbiota-dependent protection. (4) Conclusions: LBTE may serve as a complementary strategy for UC prevention and management.
(1) Background: Ulcerative colitis (UC) is a chronic inflammatory bowel disease associated with gut microbiota dysbiosis and metabolic perturbations. Although Liubao tea (LBT) has gastroprotective benefits, the precise mechanisms by which LBT extract (LBTE) alleviates UC by orchestrating microbial and metabolic homeostasis remain poorly understood. (2) Methods: A DSS-induced UC mouse model was used to evaluate LBTE efficacy. Serum pharmacochemistry, untargeted metabolomics, 16S rRNA sequencing, and targeted SCFA metabolomics were integrated to characterize absorbable active constituents, metabolic shifts, and gut microbiota landscapes. SCFA- and arachidonic acid metabolism-related targets were validated by RT-qPCR and Western blotting. PGF models and FMT were used to assess the causal role of gut microbiota in LBTE-mediated efficacy. (3) Results: LBTE preserved colon length and mucosal integrity while reducing IL-6, TNF-α, IL-1β, and oxidative stress. It enriched SCFA-producing genera and increased colonic butyric and valeric acids, activating GPR41/GPR109A signaling, upregulating ZO-1 and occludin, and strengthening the intestinal barrier. LBTE also downregulated PTGS2 and ALOX5, restored PTGS1 and CYP3A11, and inhibited NF-κB signaling. These effects were weakened in PGF mice but reproduced by FMT from LBTE-treated donors, confirming microbiota-dependent protection. (4) Conclusions: LBTE may serve as a complementary strategy for UC prevention and management.