Endothelial dysfunction plays a key role in the development of cardiovascular diseases, renal injuries and hypertension induced by hyperuricemia. Therapies targeting uric acid (UA) may be beneficial in cardiovascular diseases. In the present study, the effect of rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, was investigated to determine whether rosuvastatin improves endothelial dysfunction via the endothelial nitric oxide (NO) pathway and delays the pathogenesis of endothelial dysfunction in hyperuricemic rats. A total of 72 Sprague-Dawley rats (age, 8 weeks) were randomly divided into six groups (12 rats per group), including the control, model, 2.5 mg/kg/day rosuvastatin, 5 mg/kg/day rosuvastatin, 10 mg/kg/day rosuvastatin and 53.57 mg/kg/day allopurinol groups. The model, rosuvastatin and allopurinol rats were subjected to hyperuricemia, induced by the administration of yeast extract powder (21 g/kg/day) and oxonic acid potassium salt (200 mg/kg/day). The hyperuricemic rats were treated with 2.5, 5.0 or 10.0 mg/kg/day rosuvastatin orally for six weeks, while rats treated with allopurinol (53.57 mg/kg/day) were used as a positive control. The serum levels of NO and the gene expression levels of endothelial NO synthase in the aortic tissue increased, whereas the serum levels of UA, endothelin-1 and angiotensin II decreased in the hyperuricemic rats treated with rosuvastatin, particularly at a high rosuvastatin dose (10 mg/kg/day). In addition, the curative effect of the 10 mg/kg/day rosuvastatin group was evidently higher compared with the allopurinol group. Therefore, rosuvastatin may be a novel drug candidate for the treatment of hyperuricemia due to its endothelial protective properties.

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Background Hyperuricemia is a state in which the serum levels of uric acid (UA) are elevated. This study was to determine the roles of rosuvastatin in fasting blood glucose (FGB) and insulin levels in hyperuricemic rats. Methods Thirty-six Sprague-Dawley (SD) rats were randomized divided into the control, model and rosuvastatin groups: the control was given no intervention, the model group was established by administrating yeast extract powder and oxonic acid potassium salt, and the rosuvastatin group was given intravenous administration of rosuvastatin for 28 days in hyperuricemic rats. Serum uric acid (SUA), fasting blood glucose (FBG), fasting blood insulin (FBI), glutamic acid decarboxylase antibody (GADA), oral glucose tolerance test (OGTT) levels, and the ultrastructure of pancreatic β-cells were measured. Also, homeostasis model assessment of insulin resistance (HOMA-IR) scores was computed in three groups. Results Compared to the model group, SUA were decreased, while the FBG, GADA, OGTT and HOMA-IR at week 4 were significantly increased in rosuvastatin group. However, FBI was not significantly changed between three groups. It was also showed that the structure of pancreatic β-cells was damaged and the number of β-cells was changed in hyperuricemic rats while they were aggravated in rosuvastatin group. Conclusion Rosuvastatin has roles in inducing FGB, GADA, OGTT and pancreatic β-cells damage in hyperuricemic rats.

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Background: Hyperuricemia is the most important risk factor for gout, hypertension, coronary artery disease and other cardiovascular diseases. The incidence of hyperuricemia gradually increased in recent years and it is very necessary to explore the medications of the prevention and treatment of hyperuricemia using hyperuricemia animal models. Objective: The objective of present study is to explore the optimal dose of yeast extract and oteracil potassium in the establishment of hyperuricemia rat model. Method: Sixty-four male rats were randomly divided into 8 experimental groups. Rats were treated with yeast extract by intraperitoneal injection or yeast extract by intraperitoneal injection combined with various doses of oteracil potassium by intragastric feeding or intraperitoneal injection for 28 days. The serum uric acid, urea nitrogen and creatinine levels of different groups were measured at 0th day, 7th day, 14th day, 21th day and 28th day. Results: The serum levels of uric acid in the groups of intraperitoneal injection with yeast extract alone, yeast extract by intraperitoneal injection combined with 50-200 mg/kg oteracil potassium by intragastric feeding and yeast extract by intraperitoneal injection combined with 50-100 mg/kg oteracil potassium by intraperitoneal injection were higher than that in the control group. But we found no significant effect on rat kidney, heart or artery in the above groups. In the group of yeast extract by intraperitoneal injection combined with 200 mg/kg oteracil potassium by intraperitoneal injection, we observed the significantly high level of serum uric acid and morphological and pathological changes in rat kidney, heart and artery. Conclusion: In the present study, we found that continuously treated with yeast extract combined with oteracil potassium is an effective method to establish rat hyperuricemia model. Intraperitoneal injection of yeast extract combined with 200 mg/kg oteracil potassium is an optimal dosage for the construction of a persistent and stable hyperuricemia animal model.