It can be proposed that one of the action mechanisms of HEBP in IBD involves its ability to decrease the gene expression of TLR-4, which reduces the deregulated production of pro-inflammatory cytokines (COX-2, IL-17, TNF- α, IL-1β, and IL-6), adhesion molecules (ICAM-1), and chemokine (MIP-2 and MCP-1) due to the down-regulation of NF-κB p65. Here, NFKB1 is linked to inflammatory bowel disease.