Curcumin ameliorates DSS-induced colitis in mice by regulating the Treg/Th17 signaling pathway

Curcumin has a therapeutic effect on ulcerative colitis, but the underlying mechanism has yet to be elucidated. The aim of the present study was to clarify the possible mechanisms. Dextran sulfate sodium-induced colitis mice were treated with curcumin via gavage for 7 days. The effects of curcumin on disease activity index (DAI) and pathological changes of colonic tissue in mice were determined. Interleukin (IL)-6, IL-10, IL-17 and IL-23 expression levels were measured by ELISA. Flow cytometry was used to detect the ratio of mouse spleen regulatory T cells (Treg)/Th17 cells, and western blotting was used to measure the nuclear protein hypoxia inducible factor (HIF)-1 alpha level. The results demonstrated that curcumin can significantly reduce DAI and spleen index scores and improve mucosal inflammation. Curcumin could also regulate the re-equilibration of Treg/Th17. IL-10 level in the colon was significantly increased, while inflammatory cytokines IL-6, IL-17 and IL-23 were significantly reduced following curcumin treatment. No significant difference in HIF-1 alpha was observed between the colitis and the curcumin group. It was concluded that oral administration of curcumin can effectively treat experimental colitis by regulating the re-equilibration of Treg/Th17 and that the regulatory mechanism may be closely related to the IL-23/Th17 pathway. The results of the present study provided molecular insight into the mechanism by which curcumin treats ulcerative colitis.

Automated summary

Curcumin effectively treats ulcerative colitis by regulating the re-equilibration of Treg/Th17, reducing inflammation, and potentially involving the IL-23/Th17 pathway.