Objective To observe the preventive effect of different doses of diacerein on acute gout model rats and to explore its possible mechanism.Methods A total of 30 Wistar rats and were randomly assigned to the normal control group, the negative control (normal saline control group, and positive (colchicine) control group, diacerein low dose group, medium iddle dose group and high dose group.Except the normal control group that were given normal saline, other groups received colchicine (0.3 mg·kg-1 ·d-1), diacerein (10 mg·kg-1·d-1, 50 mg·kg-1·d-1 and 100 mg·kg-1·d-1) for 8 days respectively, and prepared acute gouty arthritis model on the 6th day, then observed rats joint swelling and gait at 2 h, 6 h, 8 h, 24 h and 48 h after the acute gouty arthritis model were established.After 48 h, the rats were killed, the serum and joint leachate of the rats were collected to test interleukin (IL)-1β and tumor necrosis factor (TNF)-α.One-way analysis of variance (ANOVA), LSD t test and Kruskal-Wallis rank sum test were used for statistical analysis.Results Compared with the normal group, joint swelling of the rats in the negative control group became significantly swollen at 2 h after the model was established,at and it reached the peak at 8 h reached the peak, then decreased gradually and remitted obviously at 48 h obviously remission.Joint swelling of the ccolchicine group and diacerein high dose group joint swelling [(0.106±0.081) cm, (0.112±0.030) cm] and ankle joint inflammation index score [(2.8±1.7), (3.16±0.75)] were significantly decreased compared with the negative control group [(0.208±0.078) cm, (4.7±1.6);P＜0.05].In addition, compared with the negative control group, the gait of diacerein high dose group was significantly improved (F=7.552, F=1.859, P＜0.05), colchieine group and diacerein high dose group, the serum and joint leaching liquid TNF-α and IL-1 levels also decreased significantly (P＜0.05).Conclusion Diacerein in any In each dosage group of has a certain preventive and therapeutic effect on rats gouty arthritis rats, especially in high dose group, the anti-inflammatory mechanism may be down-regulating the expression of proinflammatory mediators such as IL-1 beta and TNF-α.