ABSTRACT
Gastric cancer is one of the most common gastrointestinal tumors; the incidence and mortality of gastric cancer are on the increase nowadays. Helicobacter pylori [H.Pylori] causes chronic active gastritis and peptic ulcer disease. Cycloocygenase-2 [COX-2] is the central enzyme in the biosynthetic pathway to prostaglandins. Studies from different laboratories suggested that over-expression of COX-2 was detected in colon and other tumors. To obtain direct evidence concerning this relationship, we investigated the immunohistochemical findings of gastric mucosa using an animal model of gastric cancer induced by H. pylori in sprague dawley rat. The rats were randomly assigned into three groups [n=5]. Those of experimental group2 were given MNU. One week after completion of MNU administration, rats in experimental groups 1 were inoculated with H. pylori three times every other day. Rats in control group [group 3] received neither MNU nor H. pylori. Rats of groups 1, 2, and control group were maintained on standard diets throughout the experiment. Rats were weighed and sacrificed under anesthesia with ether at 20 weeks after infection. One half of the excised stomachs, were fixed in neutral-buffered 10% formalin and were cut into approximately six strips, which were processed by standard methods, embedded in paraffin, sectioned at 6 micro m, and stained with hematoxylin and eosin [H and E] and immunohistochemistry for Cox-2 protein detection. To confirm H. pylori infection, samples [3-mm[2]] of stomach mucosa transferred to appropriate medium and colonies were identified by characteristic Gram's stain morphology, and by urease, catalase, and oxidase activity sample was also placed into the gel of a rapid urease test kit. Data showed a significant decrease of animal body weight in experimental groups compared with control group. Histopathological studies showed severe infiltration of the lamina propria and submucusaal layer by polymorphonuclear and mononuclear cells appeared in the antrum, with an increase in epithelial cell proliferation, and the infiltration of focal oesophageal. Control animals showed no abnormal findings throughout the entire observation period. COX-2 protein was expressed in experimental groups but there were no evidence of cox-2 protein expression in control group. Data showed that the H. pylori caused significant decrease of body weight in experimental group. In addition, histological studies showed evidence of metaplasia in rat stomach. Immunohistochemichas studies showed cox-2 protein expression occurred during early stage of metaplasia induction