Fuzhuanbrick tea (FBT) has attracted wide attention because of its substantial nutritional value. This article first studied the protective mechanism of FBT polysaccharide (FBTP) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) by 16S rDNA amplicon sequencing technology and metabonomics. It was demonstrated that the administration of FBTP by oral gavage (100, 200, and 400 mg/kg·bw) could decrease the disease activity index (DAI), prevent colon shortening, and alleviate colon tissue damage and inflammation in mice with UC. Interestingly, FBTP relieved the intestinal microbiota disorder caused by UC and contributed to the proliferation of beneficial microbiota, such as Lactobacillus and Akkermansia, followed by a significant increase in the levels of short-chain fatty acids (SCFAs). Furthermore, FBTP dramatically altered tryptophan metabolism and elevated the fecal contents of indole-3-acetaldehyde (IAld) and indole-3-acetic acid (IAA). It was also found that FBTP significantly increased the colonic expressions of aromatic hydrocarbon receptors (AhR) and interleukin-22 (IL-22) and further promoted the expressions of intestinal tight junction (TJ) proteins ZO-1 and occludin in the colitis mice. Cumulatively, these findings suggest that FBTP can relieve UC by regulating intestinal flora disorders, promoting microbial metabolism, and repairing the intestinal barrier.

Fu brick tea theabrownin (FBTB) is a kind of biomacromolecule produced by oxidative polymerization of tea polyphenols. Although a variety of diseases can be alleviated by TB, its ability to treat ulcerative colitis (UC) is still worth exploring. A dextran sulfate sodium (DSS)-induced chronic UC mouse model was designed to first explore the alleviatory effect of FBTB on UC and its underlying mechanism by the sequencing of fecal 16S rRNA genes, metabolomics, and fecal microbiota transplantation (FMT). Administration of FBTB at 400 mg/kg bw in DSS-damaged mice could effectively reduce colonic damage and inflammation and improve colonic antioxidant capacity to relieve the UC-caused symptoms. FBTB could correct the disrupted gut microbiota caused by UC and contribute to the proliferation of Lactobacillus and Parasutterella. FMT in combination with antibiotic treatment showed that FBTB could elevate the levels of microbial tryptophan metabolites, including indole-3-acetaldehyde (IAld) and indole-3-acetic acid (IAA), by selectively promoting the growth of Lactobacillus. Importantly, FBTB-elevated IAld and IAA could activate aromatic hydrocarbon receptors (AhRs) and enhance interleukin-22 production to repair the intestinal barrier. These findings demonstrated that FBTB alleviated UC mainly by targeting the gut microbiota involved in the AhR pathway for prophylactic and therapeutic treatment of UC.