## 4 Discussion
Currently, the AhR-Nrf2 and AhR-IL-22-STAT3 pathways have been highlighted for their potential to rescue intestinal barrier defects, regulate tight junctions, and suppress gastrointestinal inflammation, particularly in inflammatory bowel disease [44]. The Nrf2 signaling pathway, known for its role in cellular defense against oxidative stress, exhibits anti-inflammatory effects by blocking pro-inflammatory cytokines and the NF-kB pathway [48; 49]. Additionally, the AhR/IL-22/STAT3 signaling pathway plays a vital role in gastrointestinal epithelial barrier function and the protection of intestinal stem cells [50; 51]. Key transcription factors, including STAT3 and suppressor of cytokine signaling (SOCS), have been implicated in the transmission of inflammatory cytokine signals [52; 53]. It has been shown that tight junctions and regulating Treg cell differentiation through the AhR/IL-22 pathway protects the colon from inflammatory damage in a mouse model of colitis, maintaining immune homeostasis [25]. Targeting these pathways is a promising strategy for the prevention and treatment of IBD. The metabolites produced by intestinal bacteria have also been recognized as integral components of AhR activation. Among these, the bacterial metabolites of tryptophan have been extensively studied, showcasing various physiological activities [54]. Additionally, polyphenols, another type of prebiotic ingredient, have garnered considerable attention as potential AhR ligands [25]. Quercetin induces a dose-dependent increase in the expression of tight junction (TJ) proteins ZO-1 and Claudin1 via the activation of AhR and CYP1A1 [25; 55]. Baialein has been shown to improve UC by enhancing the intestinal epithelial barrier through the AhR/IL-6 pathway in ILC3 [56; 57]. Metabolites of elligatnins demonstrated efficacy in mitigating colitis in preclinical models by preventing barrier dysfunction and showing their anti-inflammatory activity through the activation of the AhR-Nrf2-dependent pathway, prepulating epithelial tight junction proteins [58]. In this study, TA alone promoted AhR transcription and upregulated the expression of Nrf2, IL-22, and STAT3, while co-administration with LC resulted in a stronger induction of STAT3 and protection of tight junctions. Research suggests that targeting these pathways, including AhR regulation, holds promise for the prevention and treatment of IBD. This effect may be attributed to the ability of LC to increase the production of metabolites, such as phloroglucinol, by metabolizing TA. However, further studies are required to fully understand the relevance of these pathways in intestinal diseases. Intestinal dysbiosis and colitis are mutually correlated conditions. Studies have shown that polymerized polyphenols, including tannins, can effectively improve the intestinal flora environment and increase the abundance of bacteria like Bacteroides, Lactobacillus, Ruminococcaeae, and Akkermansia [59; 60] that produce SCFAs. The phlorotannin selected in this study has been shown to have the ability to increase SCFAs [61]. SCFAs play crucial roles in regulating intestinal immune function, protecting the intestinal mucosal barrier, reducing inflammatory responses, maintaining intestinal environment stability, and treating various conditions such as IBD, hypertension, irritable bowel syndrome, and colon cancer. Furthermore, these polyphenols are suggested as AhR ligands, modulating the intestinal immune system through the AhR pathway [25]. Additionally, phlorotannin fermentation in an in vitro rumen model increased carbohydrate-mediated bacteria, including _Prevotellaceae_UCG-001_, _Anarovonax_, _Ruminococcus_, _Ruminobacter_, _Eibroducter_, _Lachospiraceae_AC2044_group_, and _Clostridia_UCG-014_[62]. In this study, phlorotannin treatment increased the abundance of probiotics, including _F. prausnitzii_, _A. muciniphila_, _L. reuteri_, _L. casei_, and _L. plantarum_. _F.