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LI Xi, HE Hua, LIU Yao, WANG Shijun, WANG Haidong, LIU Xiaoquan. Effect of salvianolic acid A on uric acid metabolism in acute myocardial infarction rats[J]. Journal of China Pharmaceutical University, 2014, 45(3): 335-340. DOI: 10.11665/j.issn.1000-5048.20140315
Citation: LI Xi, HE Hua, LIU Yao, WANG Shijun, WANG Haidong, LIU Xiaoquan. Effect of salvianolic acid A on uric acid metabolism in acute myocardial infarction rats[J]. Journal of China Pharmaceutical University, 2014, 45(3): 335-340. DOI: 10.11665/j.issn.1000-5048.20140315
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Effect of salvianolic acid A on uric acid metabolism in acute myocardial infarction rats

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  • The aim of this study was to investigate the effect of salvianolic acid A(SalA)on uric acid metabolism in acute myocardial infarction(AMI)rats. Rats were randomly divided into Sham, AMI and SalA groups. The AMI model underwent coronary artery ligation and the survival AMI rats received a single intravenous dose of 5 mg/kg of SalA and normal saline. The uric acid plasma and myocardial concentrations, myocardial adenine nucleotides(AMP, ADP and ATP), inosine, xanthine, hypoxanthine were determined by HPLC and plasma xanthine oxidase activity was measured spectrophotometrically using commercial diagnostic kits. Myocardial infarct rate was measured by TTC dying method. After AMI, myocardial ATP depleted, the infarct rate increased and purine compounds released from necrotic cells, resulting in the increased uric acid substrate in plasma. Furthermore, the xanthine oxidase activity in plasma was increased, so the elevated substrate and increased xanthine oxidase activity resulted in elevated plasma uric acid levels. SalA increased high-energy phosphate compounds and inosine levels, reduced myocardial infarct rate, so less purine compound released to plasma. SalA also inhibited xanthine oxidase activity in plasma. Therefore, plasma uric acid was declined. The results suggested that SalA could exhibit cardiovascular protective effects by regulating of uric acid synthesis in AMI rats.
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