Wild bitter melon alleviates dextran sulphate sodium-induced murine colitis by suppressing inflammatory responses and enhancing intestinal regulatory T cells

• Wild bitter melon (WBM) intake alleviated the pathological symptoms of IBD in mice.
• WBM ameliorated colitis in mice through the ability of anti-inflammation and the capability to induce Treg cell activities.
• The ethyl acetate extract (EAE) and ethanol extract (EE) of WBM are the active fractions for the anti-inflammation activity.
• The n-butanol extract (BE) of WBM is the active fraction for the Treg cell induction activity.

The anti-inflammatory and immunomodulatory effects of wild bitter melon (WBM) on inflammatory bowel disease were investigated by using dextran sodium sulphate (DSS)-induced colitis murine model. WBM intake significantly improved weight loss, disease activity index and colon shortening. Colonic interleukin (IL)-6 and IL-1β were significantly decreased, and the anti-inflammatory cytokine IL-10 was increased in WBM-fed mice. The mRNA expression of transforming growth factor (TGF)-β and Foxp3 in colon, and Foxp3+ regulatory T (Treg) cell numbers in the mesenteric lymph nodes (MLN) were also significantly higher in the WBM group. Furthermore, ethyl acetate extract (EAE) and ethanol extract (EE) of WBM inhibited IL-6 secretion by lipopolysaccharide (LPS)-stimulated peritoneal macrophages. The n-butanol extract (BE) increased Treg cells differentiated from CD4+ T cells. This study suggested that the suppressive effect of WBM on colitis was contributed by the multiple bioactive components, at least, to inhibit inflammation and promote the development and activity of Treg cells.