Abstract

Objective: Peptic ulcer disease is a prevalent gastrointestinal disorder associated with escalating global mortality rates and a heightened risk of gastric cancer. This study investigates the therapeutic potential of Benidipine, an L-type calcium channel blocker known for its antioxidant properties, in an indomethacin-induced peptic ulcer model in rats. Methods: Thirty-six male albino Wistar rats were divided into six groups and subjected to various drug treatments, including Indomethacin, Famotidine, and Benidipine. Stomach tissue samples were collected for analysis. Results: Macroscopic examination revealed that indomethacin significantly increased ulcer areas in the stomach tissue, while Benidipine and Famotidine treatments effectively reduced these ulcer areas. Biochemical analysis indicated that Indomethacin-induced oxidative stress, as evidenced by elevated levels of malondialdehyde, a marker of lipid peroxidation, and decreased levels of total glutathione and superoxide dismutase, are crucial antioxidants. However, Benidipine treatment mitigated these changes, restoring antioxidant levels and reducing malondialdehyde levels. Conclusion: This study demonstrates that indomethacin induces gastric damage and oxidative stress, leading to ulcer formation, while Benidipine, with its antioxidant properties, effectively counteracts these effects and exhibits comparable efficacy to Famotidine in ulcer reduction. These findings suggest that Benidipine may hold promise as a therapeutic agent for mitigating peptic ulcers induced by nonsteroidal anti-inflammatory drugs like Indomethacin, warranting further exploration in clinical settings.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call