Moreover, it exerts anti-inflammatory effects by up-regulating the levels of tight junction proteins, increasing the number of goblet cells and mucin production, reducing the number of apoptotic cells, and inhibiting the MyD88/TLR4/NF-κB signaling pathway mediated by gut microbiota, thereby decreasing the injury to the intestinal mucosal barrier function brought on by DSS-induced colitis. This evidence concerns the gene NFKB1 and colitis.