To observe the effects of blood pricking therapy on serum uric acid (SUA) and the activity of related enzyme in hyperuricemic rats, and explore its mechanism. Methods:A total of 40 male SD rats were randomly divided into four groups：normal group (10 rats), model group (10 rats), allopurinol group (10 rats), and blood pricking group (10 rats). Rats with hyperuricemic were modeling by adenine and ethambutol hydrochloride intragastrically. Four weeks after successful modeling, rats in allopurinol group were lavaged allopurinol according to the body weight of rats 0.03 g/L (kg·d), 2 times/week; rats in blood pricking group were pricked for bloodletting 0.3～0.5 mL on the rats leg collaterals of the Bladder Meridian of the Foot-Taiyang and Kidney Meridian of Foot-Shaoyin until the eighth week. At the end of eighth week, the rats were made anesthesia with 10% of chloral hydrate, then 5 mL blood was draw from the abdominal aorta. By phosphoric acid method, the SUA were tested, and with enzyme-colorimetric method, the activity of the xanthine oxidase (XOD) and adenosine deaminase（ADA）were tested. Results:Compared with the normal group, the levels of SUA, ADA and XOD in the model group were significantly increased (P<0.05); compared with the model group, the levels of SUA and XOD in the allopurinol group were significantly reduced (P<0.05); the changes of SUA, ADA and XOD in the blood pricking group were significant (P<0.05). Conclusion:The blood pricking therapy can significantly inhibit the activity of XOD and ADA, reducing the level of SUA in rats with hyperuricemia.