Taurine suppresses gastric intestinal metaplasia in patient-derived organoids and Atp4a -/- mice.

Gastric intestinal metaplasia (GIM) represents a critical precancerous condition in the progression from chronic gastritis to gastric cancer, with limited therapeutic options. Emerging evidence suggests that taurine, a cytoprotective amino acid, may modulate gastric epithelial dysfunction. However, its application and efficiency in the context of GIM remain poorly understood. To investigate the therapeutic effects of taurine on GIM using patient-derived organoids and Atp4a -/- mouse models. Patient-derived GIM organoids (n = 3) and Atp4a -/- mice, which spontaneously develop GIM, were used as experimental models. Morphological changes were assessed via Alcian blue-periodic acid Schiff staining. The expression levels of the gastric epithelial marker mucin 5AC (MUC5AC) and GIM-associated markers (caudal type homeobox 2 [CDX2], MUC2, Trefoil factor family 3 [TFF3]) were quantified via quantitative PCR, Western blotting, and immunohistochemistry. We confirmed that taurine treatment significantly attenuated pathological changes, including glandular hypertrophy and vacuolar dilation, in Atp4a -/- mice. It also reduced GIM severity compared with that in the untreated model group. Under taurine treatment, MUC5AC expression was significantly increased, whereas the intestinal-specific markers CDX2, MUC2, and TFF3 were reduced (P < 0.05). In parallel, in patient-derived GIM organoids, taurine treatment significantly ameliorated GIM features, as evidenced by increased MUC5AC expression and decreased CDX2, MUC2, and TFF3 expression. This study highlights the potential application of taurine as a therapeutic agent for treating GIM, offering a promising strategy for its clinical management.