Bile Acids Develop Esophageal Cancer in a Rat Model of Duodenoesophageal Anastomosis After Total Gastrectomy

Background Gastrectomy is the most common gastrointestinal surgery in Japan。Thoracic esophageal cancer in patients who underwent surgery has a history of gastrectomy in 3–10% of cases. Whether post-gastrectomy conditions lead to esophageal carcinogenesis is controversial. This study examined whether reflux of duodenal juice to the esophagus was involved in esophageal carcinogenesis. Methods 8-week male wistar rats were exposed to duodenal content esophageal reflux. All animals underwent an esophagoduodenal anastomosis (EDA) with total gastrectomy to elicit chronic esophagitis. In ten rats sham operations were performed (Control). These rats were sacrificed at the 40th week, their esophagi were taken for hematoxylin and eosin staining and for examination of expression of COX2, oxidative stress (MDA, SOD,GSH) and bile acids in esophageal lumen and common bile duct. Results EDA showed columnar dysplasia, SCC and ADC. Total bile acids in the esophageal lumen were significantly higher in EDA compared to Control. In common bile duct, Taurocholic acid, Taurodeoxycholic acid, Taurochenodeoxycholic acid and Tauroursodeoxycholic acid in EDA are significantly higher than those in control. The mucosal MDA level of EDA was significantly higher than that of the control. GSH and SOD levels were significantly reduced in the EDA compared to the control. Lipid peroxidation in the esophageal epithelium was significantly higher in the EDA than that of control. Overexpression of COX2 was observed in dysplastic and cancer tissues. Conclusion Reflux of duodenal contents, especially bile acids, Taurocholic acid (TCA), Taurodeoxycholic (TDC) acid, Taurochenodeoxycholic acid (TCDC) and Tauroursodeoxycholic acid (TUDCA) caused oxidative stress, subsequently induces COX2, and induced esophageal carcinogenesis in EDA rat model.