Experimental antral ulcer and several protective drugs

Abstract

Antral ulcer may result from infection of Helicobacter pylori, duodenal bile reflux or gastritis. Several animal antral ulcer models were used to evaluate protection of drugs. Chemicals used to induce antral ulcer were diethyldithiocarbamate, indomethacin and strong acid solutions. Because these treatments produce damage of gastrointestinal tissues other than the antrum, most of these ulcer models cannot satisfactorily mimic the spontaneously occurring antral ulcer in human. Strong hydrochloride in refed rats also produce severe corpus lesions that might result from severe gastric oxidative stress. Oxyradical scavengers, including superoxide dismutase and allopurinol, improved antral ulcer healing. Other gastrointestinal drugs, such as prostaglandins, pirenzepine and lafutidine also were effective. Lysozyme, a mucolytic agent exerted remarkable inhibition of hemorrhagic antral and corpus ulcers in refed rats that had received strong hydrochloride. Mucolysate derived from the action of lysozyme produced elimination of gastric acid back-diffusion, which plays a pivotal role in gastric hemorrhage and antral ulceration.