Effect of glucocorticoid on IL-33 expression in esophageal carcinoma model mice and its related mechanism

Objective To investigate the effect of glucocorticoid (GC) on interleukin (IL)-33 expression in esophageal carcinoma model mice. Methods A total of 18 BALB/c mice were randomly divided into three groups such as Model group, GC group and control group. The mice in Model group drank the concentration of 100 μg/ml 4NQO solution for 16 weeks, then drank sterilized water for injection to 24 weeks; The mice in GC group were injected Dexamethasone (400 μg/mouse) into abdominal cavity for 24 weeks on the basis of the mice in Model group; The mice in Control group drank propylene glycol solution for 16 weeks, then drank sterilized water for injection to 24 weeks. All of the mice were taken blood from tail vein every four weeks. Serum levels of IL-33 were detected by enzyme linked immunosorbent assay (ELISA) method. All mice were sacrificed after 24 weeks and then the quality of intact esophagus were weighed and compared. The expression of IL-33 and ST2 protein in esophageal tissues was detected by Western blotting, and the staining of IL-33 was observed by immunohistochemistry method. Results The esophageal weight in Model group, GC group and Control group was (4.75±1.78), (2.06±0.02) and (0.08±0.01) g, respectivetly. The differences was significantly between the each group (P<0.05). The expression of IL-33 and ST2 protein, the serum level of IL-33 in Model group were significantly higher than those in GC group and Control group. The differences were statistically significant (all P<0.05). The expression of IL-33 and ST2 protein, the serum level of IL-33 in GC group were significantly higher than those in Control group. The differences were also statistically significant (all P<0.05). IL-33 staining was the most frequent in the cytoplasm of epithelial cells of esophageal mucosa in Model group A, followed by GC and Control group. Conclusion IL-33 has a significant correlation with esophageal carcinoma and GC can inhibit tumor growth by inhibiting IL-33/ST2 signal transduction pathway. Key words: Esophageal carcinoma; Interleukin-33/ST2; Glucocorticoid