WORLD JOURNAL OF ADVANCE
HEALTHCARE RESEARCH

Lina Ali*, Rana Makhous and Rana Issa

ABSTRACT

An imbalance between defensive and offensive factors leads to damage to gastric mucosal and thus ulcers. Helicobacter pylori and nonsteroidal anti-inflammatory drugs (such, indomethacin) are the most important causes of gastric ulcers. Sitagliptin is one of the antidiabetic drugs that demonstrated an anti-inflammatory and antioxidant role in many diseases. In this study, we investigated the protective effect of sitagliptin on indomethacin-induced gastric ulcers in mice and compared it with famotidine effect. Adult females Balb/c mice were divided into four groups (n=7 in each); group 1 (normal control), group 2 (induced-ulcer, non-pretreated), group 3 (sitagliptin 21 mg/kg), group 4 (famotidine 8.6 mg/kg). We administered drugs orally for 15 days, then induced gastric ulcers by a single oral dose of indomethacin (300 mg/kg). Histological findings showed that indomethacin resulted in severe damage to the gastric mucosa in mice, as histological examination showed the presence of deep ulcerations that extended through the entire mucosal membrane, damaged the muscularis mucosa and accompanied by inflammatory infiltrates. sitagliptin did not prevent or reduce the lesions caused by indomethacin, and there was a statistically significant difference between sitagliptin and famotidine. In conclusion, sitagliptin did not show a protective effect on indomethacin-induced gastric ulcers in mice.