dibai enema liquid improves ulcerative colitis by Inhibiting the Activation of Enteric Glial Cells through the S100β/RAGE/NF-κB Signaling Pathway

Emerging evidence implicates enteric glial cell (EGC) activation in ulcerative colitis (UC) pathogenesis. This study investigated how Dibai Enema Liquid (DBE) modulates EGC-mediated inflammation. LC–MS/MS qualitatively profiled DBE, and five neuroprotective constituents were docked to S100β. DBE enema efficacy was evaluated in dextran sulfate sodium–induced murine colitis by body weight, colon length, histopathology, and cytokines (ELISA); EGC activation markers were assessed by IHC, immunofluorescence co-localization, qPCR, and immunoblotting. An in vitro model used CRL-2690 enteric glia activated with lipopolysaccharide plus interferon-γ. LC–MS/MS revealed five bioactive components with strong S100βbinding. DSS increased TNF-α/IL-1β, disrupted tight junctions, and elevated S100β/GFAP at mRNA and protein levels, consistent with EGC hyperactivation; DBE significantly reversed these changes. In vitro, 15% DBE-containing drug serum reduced S100β, RAGE, iNOS (NOS2), and phosphorylated NF-κB p65. Collectively, DBE appears to alleviate UC by inhibiting EGC activation via the S100β/RAGE/NF-κB/iNOS cascade.