Compared with the model group, the protein expression of TLR4, MyD88, and NF-κB was significantly decreased in the high- and medium-dose TSD groups and the colchicine group, indicating that the effect of TSD against gouty arthritis might occur through the suppression of the TLR/MyD88/NF-κB receptor signaling pathway and the activation of inflammatory factors, the role of which was similar to the role of colchicine. The gene discussed is NFKB1; the disease is gout.