Specifically, the combination of TNF-α and its receptor TNFR-1 can promote the formation of a membrane-binding complex containing TNF receptor-associated proteins with a death domain (TRADD), TRAF, and RIPK-1 and can then mediate cell apoptosis as well as the inflammatory response involving NF-κB. In this study, the expression levels of the above proteins were upregulated in the DC group, and SC played an inhibitory role, which suggested that SC could inhibit intestinal inflammation through the TLR-4/TRIF and TNFR-1/NF-κB pathways. The gene discussed is TLR4; the disease is inflammatory response.