Curcumin ameliorated dextran sulfate sodium-induced colitis via regulating the homeostasis of DCs and Treg and improving the composition of the gut microbiota

[Display omitted] •Curcumin suppresses pro-inflammatory cytokine expression in colitis mice.•Curcumin improves the composition of gut microbiota in colitis mice.•Curcumin regulates the balance of Treg/Th17 cells in colitis mice.•Curcumin inhibits the differentiation of inflammatory DCs in colitis mice.•Curcumin regulates PI3K/Akt signaling pathway in colitis mice. Abnormal dendritic cells (DCs) and Treg cell polarisation and dysbiosis of the intestinal flora are typical features of the pathogenesis of inflammatory bowel disease (IBD). The natural compound curcumin has good anti-inflammatory properties. However, it is unclear whether curcumin effectively ameliorates IBD by regulating the homeostasis of DCs, Treg and gut microbiota. In this study, mice colitis induced by dextran sulfate sodium was orally administrated with curcumin (100 mg/kg/day) for 7 days. Consequently, the index of colonic weight significantly decreased, and body weight, colonic weight, colonic length and colonic tissue injury improved significantly; the percentage of Treg increased significantly, inflammatory DCs and pro-inflammatory cytokines decreased significantly, and the composition of gut microbiota were improved. In addition, curcumin inhibited the activation of PI3K/Akt signaling pathway in colitis mice. These data suggested that curcumin ameliorated colitis by regulating DCs, Treg and gut microbiota, and the underlying mechanism is related to PI3K/Akt pathway inhibition.