Background/Objectives: Reflux esophagitis (RE) is characterized by reflux-induced esophageal mucosal injury associated with inflammation and epithelial barrier disruption. Mineral-rich drinking water (MW) has attracted increasing attention because its mineral composition may exert various biological functions beyond simple hydration. However, its effects on reflux-induced esophageal injury remain unclear. Therefore, this study investigated the effects of MW in an acute experimental rat model of RE. Methods: The mineral composition of MW was analyzed before the animal experiment. During the 2-week acclimation period, the MW group received MW as drinking water, followed by an additional 1 mL oral administration 90 min before RE induction; ranitidine (40 mg/kg) was used as a pharmacological comparator. Gross esophageal lesions, histopathological alterations, gastric pH, mitogen-activated protein kinase (MAPK) phosphorylation, cyclooxygenase (COX) expression, and tight junction (TJ)-related proteins were evaluated. Results: MW significantly reduced gross esophageal lesions and was associated with less pronounced histopathological alterations. MW treatment was associated with lower phosphorylation levels of p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK), lower COX-2 expression, together with higher COX-1, claudin-4, and claudin-5 expression. Gastric pH was not significantly altered by MW. Conclusions: Overall, these findings suggest that MW treatment attenuates acute reflux-induced esophageal injury and is associated with changes in inflammatory signaling and TJ-related protein expression.
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Kim et al. (2026) studied this question.
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