Background:Ulcerative colitis (UC) is associated with differential expression of genes involved in inflammation and tissue remodeling,including FOXO3a,which encodes a transcription factor known to promote inflammation in several tissues.However,FOXO3a expression in tissues affected by UC has not been examined.This study investigated the effects of FOXO3a on UC pathogenesis.Methods:FOXO3a expression,in 23 patients with UC and in HT29 cells treated with tumor necrosis factor-α (TNF-α) for various durations,was detected by quantitative real-time polymerase chain reaction and West blotting analysis.Enzyme-linked immunosorbent assay was used to quantify interleukin (1L)-8 expression in FOXO3a-silenced HT29 cells treated with TNF-α for various durations.Results:The messenger RNA and protein expression of FOXO3a were significantly lower in UC tissues than those in normal subjects (P ＜ 0.01).TNF-α treatment for 0,0.5,1,6,and 24 h induced FOXO3 degradation in HT29 cells.FOXO3a silencing increased IL-8 levels in HT29 cells treated with TNF-α for 6 h (P ＜ 0.05).Conclusion:FOXO3a may play an important role in the intestinal inflammation of patients with UC.