Objective: To explore the mechanism by which Tongfeng Qingxiao Formula （TFQXF） alleviates gouty arthritis （GA） by regulating macrophage arachidonic acid （AA） metabolism and inhibiting M1 polarization. Methods: In vitro experiments: A macrophage inflammation model was induced by LPS （200 ng?mL-1） and MSU （200 μg?mL-1）. The optimal concentration of TFQXF-containing serum was screened via CCK-8 assay. Immunofluorescence （IF） detected the positive rates of inducible Nitric Oxide Synthase, CD80, CD204, and CD206. enzyme-linked immunosorbent assay （ELISA） measured protein levels of CRP, IL-1β, IL-6, TNF-α, LTs, PG, 5-LOX, and COX-2. Real-time Quantitative PCR quantified mRNA expression of 5-LOX, COX-2, and KAT5. Western blotting detected the protein expression of 5-LOX, COX-2, and KAT5; co-immunoprecipitation （Co-IP） verified the protein interactions between KAT5 and each of 5-LOX and COX-2; molecular docking technology predicted the binding energy and docking structures between proteins. In vivo experiments： A syndrome model of acute GA was established by combining a high-fat and high-sugar diet, artificial climate chamber exposure, and the classic Coderre method. Sixty male SD rats were divided into the blank group, model group, diclofenac sodium group （0.03 g?kg-1）, and TFQXF low-, medium-, and high-dose groups （11.25 g?kg-1, 22.50 g?kg-1, 45.00 g?kg-1） via random number table method, with 10 rats per group. All rats in each group received the corresponding treatment once daily for 7 consecutive days. Ankle joint diameter was measured to evaluate swelling with a vernier caliper; hematoxylin-eosin （HE） staining observed synovial tissue structure and morphology; IF staining assessed CD80 and CD206 expression in synovial tissue; ELISA detected serum levels of CRP, IL-1β, IL-6, and TNF-α in rats. Results: In vitro experiments: Compared with the LPS+MSU group, the TFQXF group significantly downregulated the fluorescence positive rates of CD80 and iNOS in macrophages （P<0.01）, but had no significant upregulating effect on the fluorescence positive rates of CD204 and CD206. Furthermore, TFQXF significantly reduced the protein expressions of CRP, IL-1β, IL-6, TNF-α, 5-LOX, COX-2, and KAT5 in macrophages （P<0.05）, and inhibited the mRNA expressions of 5-LOX, COX-2, and KAT5 （P<0.01） compared with the LPS+MSU group. In addition, in vitro experiments revealed a close interaction between KAT5 and 5-LOX, COX-2. In vivo experiments: Compared with the model group, TFQXF significantly alleviated ankle joint swelling in GA rats （P<0.05）. At 24 hours after MSU intervention, the medium- and high-dose TFQXF groups exhibited better efficacy than the low-dose group （P<0.05）. Additionally, TFQXF reduced synovial hyperplasia and inflammatory cell infiltration in the ankle joints of GA rats, downregulated serum expressions of CRP, IL-1β, IL-6, and TNF-α （P<0.05）, and significantly decreased the mean fluorescence intensity of CD80 （P<0.01） compared with the model group, but showed no significant enhancing effect on CD206 mean fluorescence intensity. Conclusion: The therapeutic effect of TFQXF on GA ankle inflammation is closely associated with inhibiting macrophage M1 polarization and regulating AA metabolism.