5-Fluorouracil attenuates dextran sodium sulfate-induced acute colitis in mice

5-Fluorouracil (5-FU) has been predominantly used in the clinic for cancer chemotherapy. Previous studies have demonstrated that 5-FU has an anti-inflammatory function. In the current study, the potential therapeutic role of 5-FU in dextran sodium sulfate (DSS)-induced acute mouse colitis was investigated. Effects on the severity of colitis were studied via histochemical and immunohistochemical staining, cytokine levels were determined by reverse transcriptoin-quantitative polymerase chain reaction and the effect of 5-FU on NF-B was examined by western blotting. Administration of 5-FU ameliorated the severity of acute DSS-induced colitis. The disease activity score was significantly lower in the 5-FU + DSS-treated mice compared with the DSS-treated group (P<0.01). Tumor necrosis factor-, interleukin-1 and interferon mRNA expression levels were significantly downregulated in the colon tissue of DSS mice treated with 5-FU compared with the untreated DSS mice (P<0.05). In addition, the number of CD4(+) T cells in the colonic lamina propria and myeloperoxidase activity were significantly decreased in the 5-FU + DSS-treated mice (P<0.05). Furthermore, 5-FU treatment significantly reduced p-NF-B-p56 protein expression levels in the colon tissue of DSS-treated mice (P<0.05). The present results demonstrated that 5-FU minimizes the abnormal immune cytokine response and relieves the pathophysiological disorders associated with experimental acute colitis. Thus, the modulating inflammatory response role of 5-FU may be partially associated with inhibiting NF-B activation and 5-FU may be a novel therapeutic strategy for the treatment of inflammatory bowel disease.