Administration of JPQCHSD suppressed TNBS-induced IBD in rats, presumably by inhibiting the oxidative stress response, neutrophil infiltration and inflammatory cytokines release induced by the overexpression of NF-κB; JPQCHSD also increased serum the content of immunoglobulin A by affecting the immune system in IBD rats, which may be contributors to the beneficial effects of JPQCHSD in the treatment of IBD (Figure 8). This evidence concerns the gene NFKB1 and inflammatory bowel disease.