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To investigate the effect of decitabine on the regulation of intestinal barrier function in mice with inflammatory bowel disease, an experimental model of colitis was established via drinking water with dextran sulfate sodium (DSS). Hematoxylin and eosin staining was used to observe the pathological changes of the colon. Cytokine production was measured by an ELISA assay. Flow cytometry was used to measure the level of regulatory T cells. Immunofluorescence, immunohistochemistry and western blot analyses detected the protein expression and distribution in colon tissue. Following the administration of decitabine, the symptoms of intestinal inflammation in the mice were significantly relieved; the expression of IL‑17 was decreased, and the levels of TGF‑β and IL‑10 were increased. In addition, the induction of forkhead box P3 (Foxp3) in naive T cells increased the proportion of CD4+ Foxp3+ T cells in CD4+ T cells. Furthermore, decitabine increased the levels of zonular occludens‑1 and occludin, and inhibited the phosphorylation of ERK1/2, JNK and p38. In conclusion, the present study suggested that decitabine could alleviate DSS‑induced impaired colon barrier and the weight loss, mucus and bloody stools in mice by releasing the inhibitory factor IL‑10, reducing the pro‑inflammatory factor IL‑17, activating CD4+ Foxp3+ T cells and inhibiting the activation of the MAPK pathway.

Decitabine attenuates dextran sodium sulfate‑induced ulcerative colitis through regulation of immune regulatory cells and intestinal barrier