Ameliorative Effect of Rosinidin Against an Ethanol-induced Ulcer: Molecular Docking and Implication of PGE2/ IL-6/IL-1β/TNF-α and NF-κB Pathways.

INTRODUCTION/OBJECTIVE: In this study, we assessed the antiulcer property of rosinidin on the Ethanol (EtOH)-induced ulcer. METHODS: EtOH was administered orally to induce ulcers in rats. The potency of rosinidin 10 and 20 (mg/kg) was evaluated under trial with EtOH-induced gastric ulcer (EtOH 1.5 ml/animal). After induction of the ulcer, rats were decapitated, and gastric contents were subjected to various biochemical estimations and histopathological examination. Furthermore, molecular docking was performed. RESULTS: Rosinidin restored gastric ulcer alterations and attenuated ulcer scores. Rosinidin modulated gastric pH and restored levels of MDA, CAT, SOD, GSH, urea, creatinine, AST, ALT, NO, PGE2, and pro-inflammatory markers. A histopathology study revealed healing and a protective effect on the stomach wall. The rosinidin showed the best binding energies at -6.061 (IL-6) and -6.275 (NF-κB) kcal/mol. DISCUSSION: Rosinidin also exhibited significant gastroprotection against alcohol-induced ulcers with oxidative stress and inflammation reduction. It has replenished antioxidant levels, reduced proinflammatory cytokines, and regulated NF-κB activity, as corroborated by positive docking outcomes. These results indicate that it can be used as a therapeutic agent for the management of gastric ulcers. CONCLUSION: Rosinidin has antiulcer properties attributed to normalizing TNF-α, PGE2, and NF-κB levels. The study suggested that rosinidin possessed favorable outcomes on EtOH-induced gastric ulcers in rats.