Objective To explore the effect of Tanshinone ⅡA on uric acid level and associated myocardial injury of hyperuri-cemia (HUA) model mice.Methods Mice were randomly divided into a control group (C group),model group (M group),Tanshinone ⅡA group (T group),and allopurinol group (A group),8 mice per group.HUA mouse model was established by daily intraperitoneal injection of potassium oxonate (350 mg/kg) and oral gavage of hypoxanthine (450 mg/kg) for 8 weeks,and Tanshinone ⅡA (6 mg/kg) or allopurinol (5 mg/kg) was administered prophylactically 1 hour in advance via oral gavage.Left ventricular function was evaluated using high-frequency echocardiography.Serum uric acid levels and xanthine oxidase (XOD) activity were measured using uric acid as-say kits and xanthine oxidase activity assay kits,and myocardial oxidative stress indicators including malondialdehyde (MDA),super-oxide dismutase (SOD),and glutathione peroxidase (GSH-Px) were assessed by ELISA.Histopathological changes were observed via HE staining,while Western blot and immunohistochemical analyses were performed to examine the expression of antioxidant-related proteins Nrf2,HO-1,and NQO-1 in myocardial tissue.Results Tanshinone ⅡA significantly reduced serum uric acid levels and XOD activity,alleviated myocardial histopathological damage,decreased MDA levels,and increased SOD and GSH-Px levels in HUA mice.Furthermore,Tanshinone ⅡA markedly upregulated the protein levels of Nrf2,HO-1,and NQO-1 in myocardial tissue and improved left ventricular function,including stroke volume,ejection fraction,and fractional shortening.Conclusion Tanshinone ⅡA lowers serum uric acid levels by regulating XOD activity and mitigates myocardial oxidative stress by activating the Nrf2 pathway,thereby improving cardiac function and alleviating myocardial histopathological damage in HUA mice.
维普
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