Effects of D-002 on aspirin-induced ulcers and neutrophil infiltration on the gastric mucosa

introduction: the gastric mucosa is susceptible to the effects of aggressive factors, which are counterbalanced by mucosal defensive factors. acid peptic diseases result from the imbalance between these aggressive and defensive factors. aspirin-induced ulcer is a model of nsaids-induced damage in which neutrophil infiltration plays a key role. objective: this paper investigates the protective effect of d-002 against aspirin-induced ulcers and associated neutrophil infiltration in the gastric mucosa. methods: rats were randomized into six groups of 8 rats each. a negative vehicle control, and five aspirin (300 mg/kg)-treated groups: a positive control, orally treated with the vehicle, three with d-002 (25, 50 and 100 mg/kg, respectively) and other with 10 mg/kg omeprazole. five hours after induced damage the rats were sacrificed. the stomachs were removed and opened, and lesions examined macroscopically and microscopically. ulcer indexes and neutrophil infiltration per ulcer areas were measured. results: all positive, none negative, controls exhibited aspirin-induced ulcers. oral treatment with d-002 (25-100 mg/kg) dose-dependently and significantly reduced aspirin-induced gastric lesions (37 to 75 %), the mean number of microscopic ulcers (40 to 72 %) and neutrophil infiltration (41.7 to 83.1 %) in the rat gastric mucosa. conclusion: oral treatment with d-002 (25-100 mg/kg) effectively protects against aspirin-induced ulcers and decreases the neutrophil infiltration in the gastric mucosa induced by aspirin ulceration.