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目的:研究黄芩甲苷对心肌缺血再灌注大鼠氧化应激反应的干预作用及其作用机制。方法:将120只大鼠随机分为6组，每组20只：假手术组(sham组)、模型组、黄芩甲苷低(10 mg/kg)、中(20 mg/kg)、高(40 mg/kg)剂量组，地尔硫n (阳性对照药)组。采用夹闭冠状动脉的方法制备心肌缺血再灌注损伤大鼠模型，连续尾静脉治疗给药7 d，给药结束后，于腹主动脉取血并分离得到血清，测定血清中谷草转氨酶(aspartate aminotransferase，AST)、磷酸肌酸激酶(phosphocreatine kinase，CPK)以及乳酸脱氢酶(lactate dehydrogenase，LDH)活性；取血结束后，每组随机取出大鼠心脏，切片，并进行2，3，5-氯化三苯基四氮唑(2，3，5-triphenyltetrazolium chloride，TTC)染色，评估各组大鼠心肌梗死面积；每组另外10只取出心脏进行匀浆得心脏组织匀浆液，比色法检测心肌组织中氧化应激因子超氧化物歧化酶(superoxide dismutase，SOD)、还原性谷胱甘肽(Glutathione，GSH)、丙二醛(malondialdehyde，MDA)、过氧化氢酶(catalase，CAT)水平；Western blot法检测心肌组织中血红素加氧酶1(heme oxygenase 1，HO-1)、新型核调节因子2(novel nuclear regulator2，Nrf2)蛋白表达并进行定量分析。n 结果:黄芩甲苷低中高剂量组大鼠心肌组织梗死面积分别为(35.02±9.36)%，(29.41±6.38)%，(25.47±6.31)%；黄芩甲苷低剂量组血清中AST的含量为(477.00±83.49)kU/L，中剂量组血清中AST的含量为(398.00±64.17)kU/L，高剂量组中AST的含量为(408.00±48.38)kU/L；CPK的含量分别降为(523.00±49.36)，(458±38.77)，(336±36.13) kU/L；LDH的含量为(901.00±89.65)，(867.00±84.04)，(695±69.55)kU/L；心肌组织中SOD活性升高为(24.43±4.35)，(27.14±3.18)，(34.96±6.46)U/g；GSH的活性升高为(11.27±4.83)，(14.70±2.49)，(15.28±3.53)U/g；CAT活性升高为(7.08±0.96)，(9.59±1.35)，(12.51±2.36)U/g；MDA的活性降低为(28.97±4.46)，(23.59±3.24)，(16.04±2.67)U/g；同时对HO-1、Nrf2蛋白表达进行检测，HO-1蛋白相对表达量升高为(1.61±0.05)，(1.73±0.03)，(2.04±0.04)U/g；Nrf2蛋白的相对表达量显著升高为(1.61±0.03)，(1.93±0.03)，(2.34±0.02)。上述数据与模型组比较，差异具有统计学意义(n P值均<0.05)。n 结论:黄芩甲苷具有抑制心肌缺血再灌注损伤大鼠氧化应激反应的作用，其作用机制可能与黄芩甲苷能够提高机体Nrf2与HO-1内源性抗氧化信号传导通路，增加心肌组织的抗氧化能力来发挥心肌保护作用。“,”Objective:To study the effect and mechanism of astragaloside on oxidative stress induced by myocardial ischemia-reperfusion in rats.Methods:Total of 120 rats were randomly divided into 6 groups with 20 rats in each group: sham operation group, model group, astragaloside (10, 20, 40 mg/kg) dose groups. Diltiazem (positive control drug) group.A rat model of myocardial ischemia-reperfusion injury was prepared by clamping the coronary arteries. Continuous tail vein treatment was given for 7 days. After administration, blood was collected from the abdominal aorta and serum was collected to determine serum aspartate aminotransferase (AST), creatine kinase (CPK) and lactate dehydrogenase (LDH) activity; At the end of blood collection, 10 hearts in each group were randomly taken out and sectioned. TTC staining was performed to assess the myocardial infarct size of each group.10 hearts in each group were homogenized to obtain cardiac homogenate, and colorimetry was used to detect myocardial tissue. Oxidative stress factors such as superoxide dismutase (SOD), reduced glutathione (GSH), malondialdehyde (MDA), and catalase (CAT) levels were tested; HO-1 in myocardial tissue and Nrf2 protein expression were quantitative analysis by Western blot.Results:The myocardial infarct area of rats in the low, middle and high dose group of baicalin were(35.02±9.36) %, (29.41±6.38)%, (25.47±6.31)%, respectively; The content of AST in serum of each group decreased to (477.00±83.49), (398.00±64.17), (408.00 ± 48.38 )kU/L; CPK content decreased to (523.00 ± 49.36), (458.00±38.77), (336.00±36.13 )kU/L; The content of LDH is (901.00±89.65), (867.00±84.04), (695±69.55 )kU/L; The increase of SOD activity in myocardial tissue was (24.43±4.35), (27.14±3.18), (34.96±6.46 )U/g; GSH activity increased to (11.27±4.83), (14.70±2.49), (15.28±3.53)U/g; CAT activity increased to (7.08±0.96), (9.59±1.35), and( 12.51±2.36)U/g; The activity of MDA decreased to (28.97±4.46), (23.59±3.24), (16.04±2.67)U/g. At the same time, the expression of HO-1 and Nrf2 proteins were reduced. The relative expression of HO-1 protein increased significantly to (1.61±0.05), (1.73±0.03), (2.04±0.04); The relative expression of Nrf2 protein was significantly increased to (1.61±0.03), (1.93±0.03) and ( 2.34±0.02). Compared with the model group, the above data have significant differences (all n P values <0.05).n Conclusion:Astragaloside has the effect of inhibiting oxidative stress induced by myocardial ischemia-reperfusion injury in rats. The mechanism may be that astragaloside can increase the endogenous antioxidation signal transduction pathway of Nrf2 and HO-1 in the body and increase the myocardial tissue.