中文摘要：

目的：观察丹参酮ⅡA对过氧化氢诱导的心肌细胞凋亡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200μmol／L过氧化氢作用2h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24h。采用流式细胞仪检测细胞凋亡率、细胞内游离钙及心肌细胞线粒体膜电位的变化，检测心肌细胞膜Na^＋ -K^＋ -ATP酶、Ca2^2＋ Mg^2＋ -ATP酶活性。结果：模型组心肌细胞经200μmol／L过氧化氢作用2h后，凋亡率显著增高。与模型组比较，丹参酮ⅡA可呈浓度依赖性显著降低细胞凋亡率。过氧化氢可导致心肌细胞内游离钙显著增加，线粒体膜电位、Na^＋ -K^＋ -ATP酶、Ca^2＋-Mg^2＋ -ATP酶活性显著降低。丹参酮ⅡA可呈浓度依赖性显著降低细胞内游离钙浓度，增加线粒体膜电位、Na^＋ -K^＋ -ATP酶、Ca^＋ -Mg^2＋ ATP酶活性。结论：丹参酮ⅡA可以抑制过氧化氢诱导的心肌细胞凋亡，这可能与其增强细胞Na^＋ -K^＋ -ATP酶、Ca^＋- Mg^2＋ -ATP酶活性，降低细胞内钙超载有关。

英文摘要：

Objective ：To study protective effect and mechanism of Tanshinone ⅡA on damage induced by hydrogen peroxide in myocardial cell. Methods ：Primary 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. Apeptosis rate, [ Ca^2＋] i and mitochondrial membrane potential was determined by flow cytometric analysis. Besides, Na^＋ - K^＋ - ATPase and Ca^2＋ - Mg^2＋ - ATPase was also evaluated in each group. Results ： In model group, apoptosis rate rose significantly compared with normal group. Comparing with model group,Tanshinone ⅡA decreased apoptosis rate in a dose dependent manner. Comparing with norreal group, [ Ca^2＋ ] i was increased remarkably, while mitochondrial membrane potential, Na^＋ -K^＋ -ATPase and Ca^2＋ -Mg^2＋ - ATPase dropped remarkably in model group. Comparing with model group,Tanshinone Ⅱ A decreased [ Ca^2＋ ] i significantly, and increased mitochondrial membrane potential,Na^＋ -K^＋ -ATPase and Ca^2＋ -Mg^2＋ -ATPase significantly in a dose dependent manner. Conclusion：Tanshinone Ⅱ A could attenuate apoptosis induced by hydrogen peroxide,the mechanism may be that Tanshi- none Ⅱ A could enhance Na^＋ - K^＋ - ATPase and Ca^＋2 - Mg^2 ＋ - ATPase activity, and thus reduce intracellular free calcium.