丹参酮ⅡA对过氧化氢损伤心肌细胞保护作用及机制探究.docVIP

丹参酮ⅡA对过氧化氢损伤心肌细胞保护作用及机制探究 　作者：杨萍，李杰，周凤华，李丽君，贾钰华 【摘要】 目的观察丹参酮ⅡA对过氧化氢诱导的心肌细胞损伤的保护作用及其机制。方法采用差数贴壁法体外分离培养新生乳鼠心肌细胞，以200 μmol/L过氧化氢作用2 h 模拟心肌细胞氧化应激模型，分别以丹参酮ⅡA高、中、低剂量在造模前干预24 h。采用MTT法检测细胞活力，流式细胞仪Annexin V-PI双染法检测细胞凋亡率，检测心肌细胞总抗氧化能力（T-AOC）、LDH活性、MDA含量、SOD活力、GSH-Px活力、CAT活力。结果模型组心肌细胞经200 μmol/L过氧化氢作用2h后，细胞活力显著降低，凋亡率显著增高。与模型组比较，丹参酮ⅡA显著增加心肌细胞活力，降低细胞凋亡率。过氧化氢可导致心肌细胞LDH活性及MDA含量显著增加，并使总抗氧化能力（T-AOC）、SOD活力、GSH-Px活力、CAT活力显著降低，丹参酮ⅡA可呈浓度依赖性显著降低LDH活性及MDA含量，增加总抗氧化能力（T-AOC）、SOD活力、GSH-Px活力、CAT活力。结论丹参酮ⅡA可以抑制过氧化氢诱导的心肌细胞损伤，这可能与其增强细胞抗氧化酶活力，降低脂质过氧化反应有关。 【关键词】 丹参酮ⅡA； 心肌细胞； 氧化应激 ChinaAbstract：ObjectiveTo study the protective effect and mechanism of Tanshinone ⅡA on myocardial damage induced by hydrogen peroxide.MethodsPrimary cultured neonate rat myocardial cell was cultured in medium with 200μmol/L hydrogen peroxide, and the medium was supplemented with different concentrations of Tanshinone ⅡA in advance. Cell viability was determined by MTT method. Annexin V/PI bivariate dyeing was used to detect apoptosis rate. Besides, T-AOC, LDH, MDA, SOD, GSH-Px, CAT were detected to evaluate cell antioxidant ability.ResultsIn model group, cell viability decreased significantly and apoptosis rate rose significantly compared with normal group. Compared with model group, Tanshinone ⅡA increased cell viability and decreased apoptosis rate in a dose-dependent manner. Compared with normal group, LDH and MDA increased remarkably, and T-AOC, SOD, GSH-Px, CAT were dropped remarkably in model group. Compared with model group, Tanshinone ⅡA decreased LDH and MDA significantly ,and increased T-AOC, SOD, GSH-Px, CAT significantly in a dose-dependent manner. ConclusionTanshinone ⅡA can reduce myocardial damage induced by hydrogen peroxide, the mechanism may be related with the enhancement antioxidase activity, and decrease of lipid peroxidation. 　　Key words：Tanshinone ⅡA; Myocardial cell; Oxidative stress 　　随着冠状动脉内溶栓、冠脉球囊扩张及冠脉搭桥等内外科治疗缺血性心脏病手段的广泛应用，在恢复缺血心肌的再灌注挽救缺血心肌的同时，缺血/再灌注( Ischemia/reperfusion, I/R)损伤所带来的问题日益明显［1］