Background: The clinical treatment of ulcerative colitis is limited. A traditional Chinese medicinal formula, Huang Qin Tang, is chronicled in Shang Han Lun and is widely used to ameliorate gastrointestinal disorders, such as ulcerative colitis; however, its mechanism is yet to be clarified.
Purpose: The present study aimed to investigate the effect of Huang Qin Tang on 7-day colitis induced by 3% dextran sulfate sodium (DSS) in mice and further explore the inhibitory effect of metabolites on DSS-damaged FHC cells.
Methods: The therapeutic efficacy of Huang Qin Tang was evaluated in a well-established DSS-induced colitis mice model. The clinical symptoms were analyzed, and biological samples were collected for microscopic examination, metabolomics, metagenomics, and the evaluation of the epithelial barrier function. The mechanism of metabolites regulated by Huang Qin Tang was evaluated in the DSS-induced FHC cell damage model. The samples were collected to detect the physiological functions of the cells.
Results: HQD suppressed the inflammation of DSS-induced colitis in vivo, attenuated DSS-induced clinical manifestations, reversed colon length reduction, and reduced histological injury. After Huang Qin Tang treatment, the DSS-induced gut dysbiosis was modulated, and the gut microbiota achieved a new equilibrium state. In addition, Huang Qin Tang activated the mTOR signaling pathway by upregulating amino acid metabolism. Significant phosphorylation of S6 and 4E-BP1 ameliorated intestinal epithelial barrier dysfunction. Moreover, Huang Qin Tang-regulated metabolites protected the epithelial barrier integrity by inhibiting DSS-induced apoptosis of FHC cells and regulating the proteins affecting apoptosis and cell-cell junction.
Conclusions: These findings indicated that the mechanism of Huang Qin Tang was related to regulating the gut microbiota and amino acid metabolism, activating the mTOR signaling pathway, and protecting the intestinal mucosal barrier integrity.