Objective:To study the effects of Qingre Lishi Prescription on ATP-P2X7R-IL-1β signaling pathway in rats with acute gouty arthritis.Methods:Otally 60 SPF-grade SD rats were divided into normal group, model group, colchicine group, and Qingre Lishi Prescription low-, medium- and high-dosage groups according to random number table method; the normal group and model group were given distilled water at a dosage of 10 ml/kg by gavage, the colchicine group was given colchicine solution at a dosage of 0.6 mg/kg by gavage, and Qingre Lishi Prescription low-, medium- and high-dosage groups were given Qingre Lishi Prescription extract suspension at dosages of 11.76, 23.52, and 47.04 g/kg by gavage, once a day for 7 consecutive days. Except for the normal group, AGA models were prepared by gavage on the 4th day in all other groups, and the swelling index of the right posterior ankle joint of rats was measured at 6, 12, 24, 48, and 72 hours after modeling; after 7 days of administration, samples were taken and HE staining was used to observe the pathological changes in the synovial tissue of the right posterior ankle joint. ELISA was used to detect the levels of serum ATP, IL-1 β, IL-8, and IL-37, and immunohistochemistry was used to detect the positive rates of P2X7R and IL-1 β proteins in the synovial tissue of the right posterior ankle joint.Results:At 6, 12, 24, 48, and 72 hours after modeling, compared with the model group, the swelling index of the colchicine group and Qingre Lishi Prescription low-dosage group decreased ( P<0.01); the levels of serum ATP, IL - β, IL-8, and IL-37 decreased in the colchicine group and Qingre Lishi Prescription low-, medium-, and high-dosage groups ( P<0.01); the expressions of P2X7R and IL-1 β proteins in the synovial tissue of the right posterior ankle was reduced in the colchicine group and Qingre Lishi Prescription high-dosage group ( P<0.05). Conclusion:Qingre Lishi Prescription may improve joint swelling and alleviate synovial tissue inflammation in AGA model rats through ATP/P2X7R/IL-1β-mediated inflammatory factor pathway.