Appearance of myofibroblasts in the gastric mucosa after ingestion of ethanol and lansoprazole with reevaluation of the mucoid cap.

The mucoid cap is important in the restitution of surface epithelial cells of the gastric mucosa. We conducted the present study to clarify the relationship of the mucoid cap and the myofibroblasts in the course of healing of the gastric mucosa with ethanol-induced damage. The effect of lansoprazole on ulcer healing was also evaluated. Wistar strain male rats were administered ethanol (50%) by gastric intubation. Thirty minutes later, either an aqueous solution of lansoprazole (LPZ; 10 mg/100 g of body weight), or the same amount of physiological saline was administered by gastric intubation. Localization of the myofibroblasts was evaluated at 1, 3, and 12 hr after LPZ treatment, and compared with the number and localization of cells positive for rhodamine-phalloidin. The concentration of basic fibroblast growth factor (FGF) was determined by EUSA. We observed PR 2D3-immunoreactive cells in the lamina propria mucosae of the control fundus that were weakly positive or negative for rhodamine-phalloidin. Erosive lesions reaching more than half of the whole gastric mucosal layer were induced 1 hr after ethanol ingestion. An abundance of PR 2D3 and rhodamine-phalloidin double-positive cells was present in the lamina propria mucosae just below the erosive lesion. The administration of LPZ brought about an increase in bFGF concentration, an acceleration of ulcer healing, and an increase in immunoreactivity to PR 2D3. In conclusion, LPZ strongly influenced the healing of gastric mucosal damage related to ethanol administration, possibly through an increase in the concentration of bFGF. The immunophenotype of the myofibroblasts changed to the muscle type during healing, suggesting an involvement of these cells in ulcer healing.