Gegen Qinlian Decoction Mitigates DSS-Induced Acute Colitis and Reinstates Gut Barrier Function in Mice, Correlating...

As a classical prescription documented in the Treatise on Febrile Diseases, Gegen Qinlian Decoction (GGQLD) has been widely utilized for diarrhea and dysentery across history. Modern research indicates its potential efficacy in inflammatory bowel diseases, including ulcerative colitis (UC).

To elucidate the pathways involved, this research examined how GGQLD reduces the severity of DSS-induced colitis in mice.

To establish acute colitis, C57BL/6J mice were exposed to 3% DSS. Different doses of GGQLD, recombinant IL-33, or an IL-33-neutralizing antibody were then administered. The expression profiles of IL-33/ST2 pathway components and epithelial barrier proteins were investigated using immunostaining, qPCR, and Western blotting. Macrophage phenotypes were evaluated by flow cytometry, and cytokine secretion was assessed by ELISA.

DSS exposure increased IL-33 expression, accompanied by a shift toward an M1-like macrophage phenotype and epithelial barrier damage. Recombinant IL-33 further exacerbated inflammation and permeability. In contrast, GGQLD and IL-33 neutralization alleviated colitis and reversed these changes. GGQLD treatment was accompanied by reduced M1-associated responses and an increased proportion of CD163⁺ M2-like macrophages, together with decreased TNF-α and elevated IL-10 levels. In parallel, restoration of β-catenin and E-cadherin expression was observed, along with reduced ST2 expression.

In a DSS-induced acute colitis mouse model, GGQLD alleviated disease severity and reduced IL-33/ST2 signaling activity. In parallel, macrophages displayed a shift toward an M2-like phenotype, accompanied by changes in inflammatory cytokine profiles and improved intestinal epithelial barrier integrity. These findings suggest that modulation of the IL-33/ST2 pathway may be involved in the therapeutic effects of GGQLD.