Weaning stress damages the intestines and disrupts the intestinal barrier in piglets, which significantly impacts the pig farming industry’s economy. We aimed to examine the effects of ShenQiGan extract (CAG) on intestinal barrier function and explore the underlying molecular mechanisms in stress-challenged weaned piglets. The experimental design involved 80 weaned piglets aged 28 days (with an average body weight of 7.78 ± 0.074 kg) that were randomly allocated into four groups: Control, LCAG (0.1% CAG), MCAG (0.5% CAG), and HCAG (1.0% CAG). After a 28-day trial period, the growth performance and incidence of diarrhea in piglets were evaluated. CAG increased the average daily gain of weaned piglets, reduced the feed-to-gain ratio, and decreased the incidence of diarrhea. It significantly lowered serum inflammatory cytokine levels while elevating immunoglobulin levels. The supplement notably enhanced concentrations of acetic acid, propionic acid, butyric acid, and isobutyric acid. Furthermore, CAG demonstrated intestinal morphology restoration and upregulation of tight junction proteins and MUC2 protein expression in jejunum. At the mRNA level, it significantly upregulated the expression of Occludin, Claudin1, and MUC2 genes. CAG improves growth performance and mitigates diarrhea in weaned piglets by enhancing intestinal barrier integrity, modulating systemic inflammatory responses, elevating immunoglobulin levels, and promoting short-chain fatty acids (SCFAs) production in the cecum.

With dysregulation of the gut microbiota and its metabolic byproducts playing a pivotal role in inflammatory bowel disease (IBD) pathogenesis. Baitouweng Tang (BTWT), a traditional herbal formulation, has long been employed to treat gastrointestinal disorders and shows promising potential in the management of IBD. However, its precise pharmacological mechanisms remain elusive. In this study, we employed targeted metabolomics, high‐throughput sequencing, and molecular biology techniques to elucidate the therapeutic mechanisms of BTWT in the treatment of ulcerative colitis (UC). BTWT significantly enhanced the relative abundance of Bifidobacterium , improved the indole metabolic pathway of tryptophan, and restored the levels of indole metabolites, such as indole‐3‐lactic acid (ILA). These changes activated the aryl hydrocarbon receptor (AhR) and led to marked improvements in the clinical symptoms of UC in mice. Conversely, the therapeutic effects of BTWT were substantially diminished in an antibiotic‐induced gut microbiota depletion model. Notably, fecal microbiota transplantation (FMT) partially restored BTWT efficacy, underscoring the critical role of the gut microbiota in mediating its therapeutic effects. Furthermore, in an in vitro lipoteichoic acid (LTA)‐induced HT‐29 inflammation model, ILA treatment attenuated inflammation and concurrently increased the expression of AhR, CYP1A1, and CYP1B1. These findings suggest a potential link between BTWT‐induced changes in tryptophan metabolites, AhR pathway activation, and the amelioration of colitis, though the causal relationship remains to be established. Our study provides a basis for further mechanistic investigation into the AhR pathway as a possible therapeutic target in UC.