Taken together, these data suggest that CK and BBR have influence on reducing LPS-stimulated pro-inflammatory cytokines, increasing anti-inflammatory cytokine expression, contributing to inhibition of the activation of NF-κB pathway, restraining p65 translocated to nucleus, and inhibiting phosphorylation of IκB of macrophage cells, which may serve as mechanism for CK down-regulated inflammatory responses of intestinal disorder in vivo. Here, NFKB1 is linked to intestinal disorder.