Abstract
Reactive oxygen species (ROS) have been implicated in the etiology of indomethacin-induced gastric mucosal damage. The protective effect of the oral administration of N-(2-Mercaptopropionyl) glycine (MPG) from oxidative gastric mucosal injury induced by the non-steroidal anti-inflammatory drug indomethacin was investigated in the rat. The total areas of the gastric lesions, as well as lipid peroxidation, were significantly increased one hour after oral administration of indomethacin (15 mg/kg) indicating an acute oxidative injury. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST) as well as glutathione (GSH) content were significantly decreased in the gastric mucosa by indomethacin. The administration of indomethacin was associated with a significant decrease in total protein and albumin contents in serum, concomitant with significant increases in glucose concentration and the activities of lactate dehydrogenase (LDH) and alkaline phosphatase (ALP) in serum. Pretreatment with MPG (2.5 mg 1kg body weight, ig) reduced gastric mucosal lesions, decreased the lipid peroxides and undermined the decrease in the activities of SOD, CAT, and GST in gastric mucosa. In addition, the administration of MPG one hour prior to the induction of gastric injury by indomethacin, abolished the indomethacin-induced decrease in total protein and albumin contents, as well as the increase in glucose concentration and the activity of LDH, but did not affect the ALP activity in serum. In conclusion, MPG has a protective potential from indomethacin-induced gastric ulceration and that the gastroprotective properties of MPG might attributed to its positive effects on the antioxidant system in indomethacin-induced gastric ulcers in rats. MPG might serve as a novel co-therapeutic agent when administered in combination with indomethacin to limit its oxidative injury.