The aetiology and pathogenesis of IBD are not very clear. In recent years, research has mainly focused on genetic susceptibility, immune abnormalities, and changes in intestinal flora. Immune factors play an important role in the occurrence and development of IBD, especially T lymphocyte subsets . In this study, a UC model was established with DSS, and the general conditions of the rats, DAI, histopathology, Treg cells and Th17 cells were analysed. It was found that curcumin could alleviate the disease course of experimental UC by regulating the balance of Treg/Th17 cells.
In this study, rats in the model group experienced weight loss, changes in faecal traits, positive faecal occult blood, and even bloody stools. Moreover, DAI and histopathological damage also changed significantly. Curcumin significantly improved the general conditions, DAI and intestinal injury of rats with UC. This finding is consistent with those of previous studies showing that curcumin can relieve intestinal inflammation. Joon-Yeop Yang et al. indicated that curcumin inhibits the severity of 3% DSS-induced inflammatory bowel disease through STAT3 . Studies have shown that curcumin can inhibit DSS-induced murine colon cancer  and can also maintain the intestinal microecological balance and the relationship between microorganisms and the host .
Recently, it was discovered that Th17 and Treg cells are CD4 + T cell subgroups that are different from Th1 and Th2 cells. Th17 cells mainly secrete IL-17A, IL-17F, IL-21, IL-22 and other cytokines, while Treg cells inhibit immune responses and mainly secrete IL-10. A large amount of evidence shows that improving the imbalance of Treg/Th17 cells is a potential strategy for the treatment of IBD . In this study, flow cytometry showed that the proportion of Treg cells in experimental UC rats was significantly lower and the proportion of Th17 cells was significantly higher than those of rats the normal group. This finding is consistent with the protective effect of Treg cells and the damaging effect of Th17 cells in autoimmune diseases .
IL-17 is a pro-inflammatory cytokine produced by T cells that can further trigger T cells and other immune cells to produce chemokines, cell adhesion molecules and other cytokines and plays a key role in the progression of IBD. In an experimental model of encephalomyelitis, it was found that the level of IL-17 and the mRNA expression of IL-17 in the curcumin treatment group were reduced, the levels of TGF-β, STAT3 and p-STAT-3 were inhibited, and the phosphorylation of STAT-3 in T cells was inhibited, blocking the differentiation of Th-17 cells . An experimental animal model of autoimmune myasthenia gravis (EAMG) showed that curcumin inhibited the expression of pro-inflammatory factors (IL-17, IFN-γ and TNF-α) and increased the expression of the anti-inflammatory cytokine IL-10, thereby reducing the clinical symptoms of EAMG in rats . The present study showed that compared with those of IBD rats in the DSS group, IL-17A levels in IBD rats in the curcumin group were significantly decreased. In conclusion, curcumin can regulate inflammation by regulating the expression of IL-17.
IL-10 is a cytokine with immunomodulatory effects that can counteract pro-inflammatory factors such as IL-2, TNF-α and IFN-γ and balance the body's inflammatory response. Many studies have shown that defects in IL-10 expression are related to the pathogenesis of IBD. Studies  have shown that curcumin can reduce the expression of the pro-inflammatory cytokines IL-1β, IL-12, IFN-γ, TNF-α and IL-1 while increasing the expression of the anti-inflammatory cytokines IL-4 and IL-10. Curcumin can also limit colitis mediated by the Th1 response in IL-10(-/-) mice and has a synergistic effect with IL-10, downregulating the activity of NF-κB in intestinal epithelial cells . Epstein et al.  showed that curcumin could increase the expression of IL-10D in the colonic mucosa of children and adults with IBD. The present study showed that compared with those of IBD rats in the DSS group, IL-10 levels of IBD rats in the curcumin group were significantly higher. Therefore, the protective effect of curcumin was related to IL-10.
In summary, curcumin attenuated colonic tissue damage in DSS-induced UC rats by improving the Treg/Th17 cell balance and influencing the expression of inflammatory cytokines.