1Assistant Professor, Vaagdevi Institute of Pharmaceutical Sciences, Bollikunta village, Khila Warangal Mandal, Khammam-Warangal Highway, Warangal-506005, Telangana, India
2Assistant Professor, Shree Ambabai Talim Santha, Diploma College of Pharmacy, Wanlesswadi, Miraj-Sangli Road, Miraj, District - Sangli, Maharashtra 416414, India
3Professor & HOD, KM College of Pharmacy, Madurai, Tamilnadu-625107, India
4Assistant Professor, School of Pharmacy, Dhanalakshmi Srinivasan University, Samayapuram, Trichy - 621112, India
5Assistant Professor, Chandigarh College of Pharmacy, Chandigarh Group of Colleges Jhanjeri, Mohali, Punjab 140307, India
6Professor, Department of Biotechnology and Bioengineering, School of Biosciences and Technology, Galgotias University, Greater Noida, U.P, India
7Associate Professor, University School of Pharmaceutical Sciences, Rayat Bahra University, Mohali, Punjab, India
8Professor, Parul College of Pharmacy and Research, Faculty of Pharmacy, Parul University, Ahmedabad Campus, Ahmedabad, India
The widespread clinical utility of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) is severely limited by their propensity to induce gastric mucosal injury through the suppression of cytoprotective prostaglandins and the generation of oxidative stress. The present study evaluated the gastroprotective and anti-ulcerogenic efficacy of L-Arginine, a physiological precursor of nitric oxide (NO), against Indomethacin-induced gastric ulcers in Wistar rats. Experimental animals were divided into five groups and pretreated with varying doses of L-Arginine or the standard proton pump inhibitor, Omeprazole, prior to a single oral challenge with Indomethacin (30 mg/kg). The assessment included macroscopic determination of the Ulcer Index, biochemical analysis of gastric juice (pH, free and total acidity), and evaluation of mucosal defense factors (mucin and pepsin content), substantiated by histopathological examination. Results demonstrated that Indomethacin administration triggered severe hemorrhagic lesions, hyperacidity, and significant depletion of the mucus barrier. Conversely, pretreatment with L-Arginine significantly (P<0.01) and dose-dependently attenuated gastric mucosal damage, reducing the Ulcer Index and suppressing aggressive proteolytic pepsin activity. Furthermore, L-Arginine therapy effectively restored gastric pH towards neutrality and preserved glandular mucin content, exhibiting efficacy comparable to the standard drug Omeprazole. Histological analysis corroborated these findings, revealing preserved mucosal architecture with reduced submucosal edema and minimal leukocyte infiltration. These findings suggest that L-Arginine exerts a potent cytoprotective effect, likely mediated by the modulation of the nitric oxide pathway, which enhances mucosal perfusion and fortifies the epithelial barrier against NSAID-induced gastropathy.
Keywords: L-Arginine; Indomethacin; Gastric Ulcer; Nitric Oxide; Mucin; Cytoprotection.
How to cite this article: Fatima SH, Snehal, Gopinath N, Kavitha V, Barwal A, Jha AK, Sudan P, Panchal I. Evaluation of the anti-ulcer activity of L-arginine against indomethacin-induced gastric ulcer in rats. Int J Drug Deliv Technol. 2026;16(6s): 491-499; DOI: 10.25258/ijddt.16.6s.52
Source of support: Nil
Conflict of interest: None