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丹酚酸A对急性心肌缺血大鼠尿酸代谢的影响
引用本文:李茜,何华,刘瑶,王世俊,王海东,柳晓泉. 丹酚酸A对急性心肌缺血大鼠尿酸代谢的影响[J]. 中国药科大学学报, 2014, 45(3): 335-340
作者姓名:李茜  何华  刘瑶  王世俊  王海东  柳晓泉
作者单位:中国药科大学药物代谢动力学研究中心;中国药科大学药物代谢动力学研究中心;中国药科大学药物代谢动力学研究中心;中国药科大学药物代谢动力学研究中心;中国药科大学药物代谢动力学研究中心;中国药科大学药物代谢动力学研究中心
基金项目:国家自然科学基金资助项目(No.81273588)
摘    要:通过结扎大鼠冠状动脉左前降支建立急性心肌缺血大鼠模型,考察丹酚酸A对急性心肌缺血大鼠尿酸代谢的影响。大鼠随机分为3组,分别为假手术组、结扎组及丹酚酸A组(5 mg/kg)。测定血浆及心肌组织中尿酸含量,同时测定血浆黄嘌呤氧化酶活性,心肌组织中高能磷酸化合物及嘌呤化合物含量,以及心肌组织缺血率。结果表明,急性心肌缺血发生后,心肌组织中ATP耗竭,心肌组织缺血率增加,细胞坏死嘌呤化合物释出进入循环系统,心肌组织中嘌呤化合物减少。血浆中尿酸底物及黄嘌呤氧化酶活性增加,共同造成血浆尿酸水平升高。丹酚酸A可增加高能磷酸化合物及嘌呤化合物含量,减小心肌缺血率,减少细胞坏死,同时抑制血浆中黄嘌呤氧化酶活性,从两个方面减少血浆中尿酸生成。提示丹酚酸A可通过调节尿酸的生成发挥心血管保护作用。

关 键 词:丹酚酸A;尿酸;急性心肌缺血;黄嘌呤氧化酶

Effect of salvianolic acid A on uric acid metabolism in acute myocardial infarction rats
LI Xi,HE Hu,LIU Yao,WANG Shijun,WANG Haidong and 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
Authors:LI Xi  HE Hu  LIU Yao  WANG Shijun  WANG Haidong  LIU Xiaoquan
Abstract: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.
Keywords:Salvianolic acid A   uric acid   acute myocardial infarction   xanthine oxidase
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