Background: The imbalance of Treg/Thl7 cells and inflammatory injury are believed to be involved in the development of ulcerative colitis (UC). Meanwhile, 6-gingerol has been reported to alleviate intestinal inflammatory damage in mice models, but the underlying mechanism remains elusive.
Methods: In this study, dextran sulfate sodium (DSS)-induced colitis mice models were established to examine the effects of 6-gingerol on IL-17 and IL-10 secretion, and the activation of NF-κB signaling was evaluated using enzyme-linked immunosorbent assay (ELISA), Western blotting, and immunohistochemistry.
Results: 6-gingerol could significantly reduce the weight loss caused by DSS in mice models (P<0.05), which is similar to the therapeutic drug, mesalazine. Immunohistochemistry showed that 6-gingerol can repair the damaged glandular structure gradually caused by DSS, significantly decrease the IL-17 level, and increase IL-10 level in bowel tissue. ELISA revealed that 6-gingerol could significantly decrease the IL17 level and increase IL-10 level in both serum and bowel tissue, and the differences were all statistically significant (P<0.05). In addition, 6-gingerol could suppress the phosphorylation level of IκBα and p65, which was up-regulated by DSS. Further analysis with immunohistochemistry indicated p-p65 staining was mainly in the nucleus with some in the cytoplasm after DSS treatment, and the treatment with 6-gingerol could significantly weaken the density of p-p65 both in the cytoplasm and nucleus.
Conclusions: Our study suggests that 6-gingerol may alleviate inflammatory injury in UC mice by regulating NF-κB signaling pathway.
Keywords: 6-gingerol; IL-10; IL-17; NF-κB; Ulcerative colitis (UC); inflammatory injury.