Phytogenic compounds with
anti-oxidant and anti-inflammatory properties, such as
ginsenoside metabolite compound K (CK) or
berberine (BBR), are currently discussed as promising complementary agents in the prevention and treatment of
cancer and
inflammation. The latest study showed that
ginsenoside Rb1 and its metabolites could inhibit TNBS-induced
colitis injury. However, the functional mechanisms of anti-
inflammation effects of
ginsenoside, particularly its metabolite CK are still not clear. Here, using
dextran sulfate sodium (DSS)-induced
colitis in mice, clinical parameters, intestinal integrity, pro-inflammatory
cytokines production, and signaling pathways in colonic tissues were determined. In mild and sever
colitis mice, CK and BBR (as a positive agent) alleviated
colitis histopathology injury, ameliorated
myeloperoxidase (MPO) activity, reduced pro-inflammatory
cytokines production, such as,
IL-6, IL-1β, TNF-α, and increased anti-inflammatory
cytokine IL-10 production in both mice colon tissues and blood. Nevertheless, the results revealed that CK and BBR inhibited NF-κB p65 nuclear translocation, downregulated p-IκBα and upregulated IκBα, indicating that CK, as well as BBR, suppressed the activation of the NF-κB pathway in the progression of
colitis with immunofluorescence, immunohistochemical and western blotting analysis. Furthermore, CK inhibited pro-inflammatory
cytokines production in LPS-activated macrophages via down-regulation of NF-κB signaling pathway. Taken together, our results not only reveal that CK promotes the recovery of the progression of
colitis and inhibits the inflammatory responses by suppressing NF-κB activation, but also suggest that CK downregulates intestinal
inflammation through regulating the activation of macrophages and pro-inflammatory
cytokines production.