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.