Pharmacological Evaluation of Stachydrine Supporting Multi-Pathway Intervention in Gastric Ulcer Disease

Abstract

Gastric ulcer is a multifactorial disorder resulting from an imbalance between aggressive factors and mucosal defense mechanisms, with oxidative stress, inflammation, and excessive gastric acid secretion playing central roles in tissue injury. The present study evaluated the gastroprotective potential of leonurine using ethanol-induced and pyloric ligation ulcer models in mice. Gastric lesions were induced by absolute ethanol, while pyloric ligation was performed to assess gastric secretory parameters. Leonurine (10 and 20 mg/kg) was administered orally, and its effects were compared with the standard drug Omeprazole. Ulcer index, gastric pH, gastric fluid volume, and oxidative stress markers, including glutathione (GSH) and nitric oxide (NO), were evaluated. Leonurine produced dose-dependent gastroprotection, reducing ulcer severity by up to 80% and significantly preserving mucosal integrity. In the pyloric ligation model, leonurine elevated gastric pH and reduced gastric fluid volume, indicating moderate antisecretory activity. Ethanol exposure caused marked oxidative imbalance, characterized by depleted GSH and elevated NO levels, whereas leonurine restored antioxidant level and normalized NO concentrations. These findings suggest that leonurine mitigates gastric mucosal injury through antioxidant and anti-inflammatory mechanisms, along with partial suppression of gastric acid secretion. Leonurine demonstrated significant gastroprotective effects through multi-targeted mechanisms. Given its ability to restore oxidative balance and improve gastric physiology, leonurine may represent a promising natural therapeutic candidate for gastric ulcer management. Further mechanistic and clinical investigations are required to confirm its protective efficacy and elucidate its molecular targets.