Theabrownin protected intestinal barrier and improved ulcerative colitis by modulating gut microbiota
Theabrownin (TB) is a biomacromolecule formed by oxidative polymerization of tea polyphenols, and is one of the most active and abundant pigments in fuzhuan brick tea (FBTB). Using dextran sulfate sodium (DSS)-induced chronic ulcerative colitis (UC) mice model, we first explored the alleviation effect of TB on UC and further investigated its underlying mechanism by the sequencing of faecal 16S rDNA genes, metabonomics and faecal microbiota transplantation (FMT). Our results indicated that oral administration of FBTB (400 mg/kg) could effectively relieve the symptoms caused by colitis, reduce colonic damage and inflammation, and improve colonic antioxidants capacity. FMT combined 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 promoting the growth of Lactobacillus and Enterorhabdus selectively. Importantly, FBTB-elevated IAld and IAA could activate aromatic hydrocarbon receptors (AhR) and enhance interleukin-22 (IL-22) production to repair the intestinal barrier. Conclusively, our results demonstrated that FBTB alleviates UC mainly by targeting the intestinal microbiota involves the AhR pathway, which should be considered as a candidate pathway for prophylactic and therapeutic treatment for UC.
Theabrownin (TB) is a biomacromolecule formed by oxidative polymerization of tea polyphenols, and is one of the most active and abundant pigments in fuzhuan brick tea (FBTB). Using dextran sulfate sodium (DSS)-induced chronic ulcerative colitis (UC) mice model, we first explored the alleviation effect of TB on UC and further investigated its underlying mechanism by the sequencing of faecal 16S rDNA genes, metabonomics and faecal microbiota transplantation (FMT). Our results indicated that oral administration of FBTB (400 mg/kg) could effectively relieve the symptoms caused by colitis, reduce colonic damage and inflammation, and improve colonic antioxidants capacity. FMT combined 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 promoting the growth of Lactobacillus and Enterorhabdus selectively. Importantly, FBTB-elevated IAld and IAA could activate aromatic hydrocarbon receptors (AhR) and enhance interleukin-22 (IL-22) production to repair the intestinal barrier. Conclusively, our results demonstrated that FBTB alleviates UC mainly by targeting the intestinal microbiota involves the AhR pathway, which should be considered as a candidate pathway for prophylactic and therapeutic treatment for UC.