Naoki Hashimoto1. 1. Naoki Hashimoto, Department of Surgery, Kinki University, Osaka 589-8511, Japan.
Abstract
AIM: To examine the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in rat esophageal lesions induced by reflux of duodenal contents. METHODS: Thirty 8-week-old 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 with only a midline laparotomy were performed (Control). The rats were sacrificed at the 40(th) week, their esophagi were taken for hematoxylin and eosin staining and for examination of expression of COX2, PGE2, and proliferating cell nuclear antigen (PCNA), and total bile acids in the esophageal lumen was measured. RESULTS: After 40 wk of reflux, columnar dysplasia, squamous cell carcinoma and adenocarcinoma were observed. Total bile acids in the esophageal lumen were significantly increased in the EDA group compared with the sham operated rats. PCNA labelling index and esophageal tissue PGE2 levels were higher in dysplastic and cancer tissues than in control tissues. Overexpression of COX2 was observed in dysplastic and cancer tissues. CONCLUSION: Reflux of duodenal contents induces COX2 expression and increases prostaglandin synthesis in dysplastic and cancer tissues. This result suggests a possible mechanism by which bile acids promote esophageal cancer.
AIM: To examine the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in ratesophageal lesions induced by reflux of duodenal contents. METHODS: Thirty 8-week-old 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 with only a midline laparotomy were performed (Control). The rats were sacrificed at the 40(th) week, their esophagi were taken for hematoxylin and eosin staining and for examination of expression of COX2, PGE2, and proliferating cell nuclear antigen (PCNA), and total bile acids in the esophageal lumen was measured. RESULTS: After 40 wk of reflux, columnar dysplasia, squamous cell carcinoma and adenocarcinoma were observed. Total bile acids in the esophageal lumen were significantly increased in the EDA group compared with the sham operated rats. PCNA labelling index and esophageal tissue PGE2 levels were higher in dysplastic and cancer tissues than in control tissues. Overexpression of COX2 was observed in dysplastic and cancer tissues. CONCLUSION: Reflux of duodenal contents induces COX2 expression and increases prostaglandin synthesis in dysplastic and cancer tissues. This result suggests a possible mechanism by which bile acids promote esophageal cancer.
Entities:
Keywords:
Bile acids; Cyclooxygenase-2; Esophageal cancer; Esophagoduodenal anastomosis; Prostaglandin E2