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Войти в исследования World journal of gastrointestinal oncology · 2026
Taurine suppresses gastric intestinal metaplasia in patient-derived organoids and Atp4a -/- mice.
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Liu Ke, Zhang Xi, Li Fa-Zhan, Zheng Peng-Yuan, Mi Yang
Аннотация
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 Atp4a -/- mouse models.
METHODS: 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.
RESULTS: 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.
CONCLUSION: This study highlights the potential application of taurine as a therapeutic agent for treating GIM, offering a promising strategy for its clinical management.
AIM: To investigate the therapeutic effects of taurine on GIM using patient-derived organoids and Atp4a -/- mouse models.
METHODS: 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.
RESULTS: 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.
CONCLUSION: This study highlights the potential application of taurine as a therapeutic agent for treating GIM, offering a promising strategy for its clinical management.