[Reflux of bile induces esophageal mucosal inflammation and apoptosis in rats]

To investigate the esophageal mucosal inflammation and apoptosis induced by reflux of different duodenal or bile in rats.

Esophagus division in esophagogastric junction and then esophagoduodenostomy were performed on rats to make the models of duodenogastroesophageal reflux (DGER). Three kinds of reflux model, DGER (Group A), duodenoesophageal reflux without gastric juice (Group B) and DGER without bile (Group C) were made by adjusting the DGER models. 9 weeks after operation, the esophageal mucosal inflammation was examined under microscope, and the esophageal apoptosis was tested by DNA fragmentation in situ using TdT-mediated dUTP biotin nick end labling (TUNEL). Immunohistochemical method was used to detect the status of esophageal Fas protein (CD95) associated apoptosis.

Evidences of reflux esophagitis were seen in all rats with different reflux models. Esophageal inflammation was most severe in group A, then in group B, and the slightest in group C. Barrett's esophagus was seen in group A and group B but not in group C, and the incidence was found to be of no difference between the A and B groups (P > 0.05). Esophageal mucosal apoptosis index in group A was (7.05 +/- 1.44)%, being significantly higher than that in group B (5.25 +/- 1.78)% and group C (2.84 +/- 1.36)%, (P < 0.01). The apoptosis index was significantly higher in group B than in group C (P < 0.01). Fas protein was negative in normal tissues and in all injured esophageal mucosal tissues.

The DGER without bile inflicts the slighest injury on the esophageal mucosa. Bile may play a significant role in the induction of Barrett's esophagus. The apoptosis indices increase in groups A, B and C, but apoptosis is not correlated with Fas expression.