Effect of Modified Xuanfu Daizhe Decoction on Intestinal Metaplasia and Expression of CDX2 and DLK1 in Rats with Chronic Esophageal Mucosal Injury Induced by Non-acid Reflux
TANG Li-ming,SONG Ning,ZHANG Gui-xian
Abstract:
Objective Duodenal-esophageal anastomosis (total gastrectomy) was used to establish a rat model of duodenal-esophageal non-acid re.ux. The effects of Modi.ed Xuanfu Daizhe Decoction (MXDD) on esophageal intestinalization, CDX2 and DLK1 expression were observed. Methods Eighty adult male Wistar rats were randomly divided into sham-operated group, model group, MXDD group and aluminum magnesium carbonate tablet (Daxi) group, 20 rats in each group. Except for the sham-operated group, the other three groups used duodenoesophageal anastomosis (total gastrectomy) to establish the rat duodenal-esophageal non-acid re.ux model. At 25 weeks, the rats in MXDD group were given MXDD (equivalent to 30 g crude drug/kg),once a day for 3 weeks; the rats in Daxi group were orally given Daxi liquid (300 mg/kg), once a day for 3 weeks; the rats in model group were given distilled water of the same volume, once a day for 3 weeks.After 3 weeks of treatment, the thoraco-abdominal cavities of four groups of animals were opened under anesthesia, and the lower esophageal segment and anastomotic segment were cut, and longitudinal dissection was made for general observation. The tissue adjacent to anastomotic opening at the lower end of the esophagus was stained with HE to observe the pathological changes of esophagus. The histopathology of the esophagus was examined and scored. In addition, CDX2 and Notch signal molecule DLK1 were stained by immunohistochemistry to observe their expression. Results Gross observation showed that the lower esophagus of the model group was signi.cantly thicker, the lower esophagus was signi.cantly thicker, the lower esophagus mucosa was widely irregular bulge, and the appearance color was white spot. The gross pathology of esophagus in MXDD group was signi.cantly lighter than that in model group, while that in Daxi group was slightly lighter than that in model group. The incidence of mild, moderate and severe esophagitis in the model group was 2/15 (13.33%), 3/15 (20.00%) and 10/15 (66.67%) respectively, and 11/17 (64.70%), 3/17 (17.65%) and 3/17 (17.65%) in MXDD group were signi.cantly lower than those in the model group (P < 0.05), and 3/16 (18.75%), 4/16 (25%), 9/16 (56.25%) respectively. There was no signi.cant difference in the model group (P > 0.05). The incidence of Barrett esophagus was 7/15 (46.7%) in the model group and 2/17 (11.8%) in the MXDD group, which was significantly lower than that in the model group (P < 0.05), and 7/16 (43.8%) in the Daxi group (P > 0.05). The expression of CDX2 and DLK1 in the MXDD group was signi.cantly lower than that in the model group (P < 0.05), but there was no signi.cant difference between the Daxi group and the model group (P > 0.05). Conclusion MXDD can inhibit intestinal metaplasia and reduce Barrett esophagogenesis caused by non-acid re.ux by inhibiting the expression of CDX2 and Notch signaling molecule-DLK1.
