Comparative effects of combined omeprazole and dose-escalated striatin therapy versus monotherapy on VEGF, ITF, gastric ulcer area, epithelial thickness, and inflammatory response in rats with aspirin-induced gastric injury

Introduction Aspirin-induced gastritis results from reduced prostaglandin synthesis and increased oxidative stress, compromising gastric mucosal integrity. While omeprazole effectively suppresses gastric acid secretion, it does not directly promote mucosal regeneration. Striatin, a bioactive fraction of Channa striata , has anti-inflammatory and regenerative properties and may enhance mucosal healing. Purpose This study aimed to evaluate whether adjunctive striatin at escalating doses enhances the therapeutic effect of omeprazole in aspirin-induced gastric injury. Methods A controlled experimental study was conducted in 30 male Wistar rats randomly assigned into six groups (n = 5 each): healthy control, negative control, omeprazole monotherapy (20 mg/kg BW), and three combination groups receiving omeprazole plus striatin (500, 1,000, and 1,500 mg/kg BW). Gastric injury was induced using aspirin. Vascular endothelial growth factor (VEGF; day 2) and intestinal trefoil factor (ITF; day 14) were measured as markers of angiogenesis and epithelial restitution, respectively. Histological and macroscopic assessments were performed at the end of treatment. Results and Discussion VEGF levels did not significantly differ across groups. In contrast, ITF significantly increased in the highest-dose striatin group (1,500 mg/kg BW, p = 0.007), which also demonstrated improved epithelial thickness, reduced ulcer area, and lower inflammation scores. Lower doses did not produce significant changes in ITF levels. Conclusion Adjunctive striatin, particularly at higher doses, enhances gastric mucosal healing primarily through epithelial restitution rather than angiogenesis. These findings suggest potential adjunctive benefits, although further studies are needed to establish optimal dosing and clinical relevance.