To study the effect of rosuvastatin on hyperuricemia rats and their endothelial dysfunction. 72 male SD rats were randomly grouped, and a hyperuricemia animal model was established by intraperitoneal injection of yeast extract and oxonic acid potassium salt. By setting up the treatment with allopurinol as positive control, the hyperuricemia rats were treated with various doses of rosuvastatin, the levels of Uric Acid (UA), Nitric Oxide (NO), Endothelin 1 (ET-1) and Angiotensin II (Ang II) were detected in serum using commercially available detection kits and the protein expression level of endothelial NO synthase (eNOS) was detected in tissue specimens of aorta by immunohistochemistry. The results show that, compared to the normal control, the serum levels of UA, ET-1 and Ang II of hyperuricemia rats are increased while the serum level of NO and the eNOS expression in tissue specimens of aorta, as an important profile for altered endothelial function of the experimental animal model are decreased. After treatment of the animal model with rosuvastatin, it is found that the drug has improved the profile of endothelial function, which has gradually recovered to the normal level, and the curative effect is significantly higher than the allopurinol group (positive control) at the dosage of 10mg/(kg·d) and intervention time of 6 weeks, as compared to the normal control group, with significant differences from the animal model without treatment. The results suggest that the rosuvastatin treatment can improve the profile of endothelial function via recovering the serum levels of ET-1, Ang II and NO, eNOS induced by hyperuricemia, and the effect is enhanced in a dose-dependent manner.