Inhibition of DNA damage with the activation of gastric mucosal protection and gastric carcinogenesis

点击翻译按钮获取中文摘要

We hypothesized that gastric carcinogenesis may controlled by the balance of the host defense mechanism and offense by carcinogen like a mechansisms of gastric formation. We tested Rebamipide in ENNG-induced mouse duodenal carcinogenesis. ENNG was administered to the C57B1/6 mice at a concentration of 100 mg/L for 4 weeks. Then, the mice were given Rebamipide (20 or 50mg/kg) for 16 weeks. In the 16th week of the experiment, the mice were killed and the duodenum and stomach were resected. Duodenal tumors were examined by stereomicroscopy, and their incidence and size were recorded. The incidence of duodenal tumors in mice treated with ENNG,ENNG plus 20mg/kg Rebamipide and ENNG plus 50mg/kg Rebamipide was 66.7%, 58.1% and 45.2% respectively. The difference between the group treated with ENNG and the group treated with ENNG plus Rebamipide was not significant.Male wistar rats were given MNNG at a concentration of 80 mg/L for 28 weeks. Rebamipide was administered. In the 48th week of the expriment, the glandular stomach was examined for macroscopic tumors and histological examination were recorded. The incidence of gastric carcinogenesis in the group treated with MNNG and MNNG plus 20mg/kg Rebamipide was 76.9% and 61.5%, respectively. The incidence between the both groups were not significantly different. In the histological study of gastric tumors, the incidence of carcinoma and adenoma in the MNNG and MNNG Plus Rebamipide treated group were 69.2% and 30.7% respectively. The defference between these groups were significant (p<0.05).