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

[BACKGROUND] 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.

[AIM] To investigate the therapeutic effects of taurine on GIM using patient-derived organoids and mouse models.

[METHODS] Patient-derived GIM organoids ( = 3) and mice, which spontaneously develop GIM, were used as experimental models. Morphological changes were assessed Alcian blue-periodic acid Schiff staining. The expression levels of the gastric epithelial marker mucin 5AC () and GIM-associated markers (caudal type homeobox 2 [], , Trefoil factor family 3 []) were quantified quantitative PCR, Western blotting, and immunohistochemistry.

[RESULTS] We confirmed that taurine treatment significantly attenuated pathological changes, including glandular hypertrophy and vacuolar dilation, in mice. It also reduced GIM severity compared with that in the untreated model group. Under taurine treatment, expression was significantly increased, whereas the intestinal-specific markers , , and were reduced ( < 0.05). In parallel, in patient-derived GIM organoids, taurine treatment significantly ameliorated GIM features, as evidenced by increased expression and decreased , , and expression.

[CONCLUSION] This study highlights the potential application of taurine as a therapeutic agent for treating GIM, offering a promising strategy for its clinical management.