槲皮素和黄芪甲苷对大鼠缺氧心肌细胞的保护作用

目的 了解并比较槲皮素、黄芪甲苷对体外培养的缺氧心肌细胞的保护作用，寻找其作用的量效关系。方法 将SD乳鼠心肌细胞分成单纯缺氧组（A组）、缺氧＋100mg／L槲皮素组（B组）、缺氧＋50mg／L槲皮素组（c组）、缺氧＋25mg／L槲皮素组（D组）、缺氧＋50．0mg／L黄芪甲苷组（E组）、缺氧＋25．0131mg／L黄芪甲苷组（F组）、缺氧＋12．5mg／L黄芪甲苷组（G组）、缺氧＋10mg／L维生素E组（H组）。各组细胞原代培养后先加入相应浓度的槲皮素、黄芪甲苷、维生素E，再行缺氧处理12h（A组培养后直接行缺氧处理）。检测各组心肌细胞活力和乳酸脱氢酶（LDH）、丙二醛（MDA）、超氧化物歧化酶（SOD）、活性氧（ROS，只检测A、C、F、H组）值。结果B～G组与A组比较，LDH、MDA、ROS（C、F组）值下降，心肌细胞活力、SOD值上升，作用普遍优于H组。在同等高、中、低浓度下，加入黄芪甲苷组的心肌细胞活力和LDH水平总体优于加入槲皮素组（如C、F组的心,肌细胞活力为0．454±0．018、0．471±0．017，LDH为2800±9、2312±52），但两组MDA、SOD和ROS值比较，差异无统计学意义（C、F组的ROS为16．0±5．3、22．4±8．7，P〉0．05）。结论 黄芪甲苷、槲皮素能有效保护缺氧心肌细胞，减轻损伤程度，其作用优于维生素E。黄芪甲苷的保护作用较槲皮素更好，但两者减轻细胞脂质过氧化损伤的作用差异不明显。

Protective effects of Astragaloside and Quercetin on rat myocardial cells after hypoxia

OBJECTIVE: To investigate and compare the protective effects of Astragaloside IV (AST) and Quercetin (QUE) on rat myocardial cells after their exposure to hypoxia, and to determine their dose-effect relationship. METHODS: Myocardial cells from fetal SD rat were cultured in vitro and divided into 7 groups: i.e. A (hypoxia), B (hypoxia and 100 mg/L of QUE), C (hypoxia and 50 mg/L of QUE), D (hypoxia and 25 mg/L of QUE), E (hypoxia and 50.0 mg/L of AST), F (hypoxia and 25.0 mg/L of AST), G (hypoxia and 12.5 mg/L AST) H(hypoxia and 10 mg/L of VitE) groups. Different doses of AST and QUE were added into the culture media cells in each group before the myocardial cells receiving hypoxia for 12 hrs. The number of viable cells (CCK-8) and the content of lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA), active oxygen (ROS, with detection only in A, C, F and H groups) were determined after hypoxia. RESULTS: The amount of LDH, MDA, ROS (C, F groups) in group B - G decreased significantly compared with those of group A, while the number of viable cells and the SOD content increased significantly. The protective effects were better in group B - G than that of the group H. With the same dosage, levels of LDH, CCK-8 in AST-treated groups were significantly lower than those in QUE-treated group (the number of viable cells in group C, F was 0.454 +/- 0.018, 0.471 +/- 0.017, and the content of lactate dehydrogenase was 2800 +/- 9,2312 +/- 52). There were no siginificant differences in MDA, SOD and ROS levels between AST and QUE treated groups (ROS in C and F groups were 16.0 +/- 5.3 vs 22.4 +/- 8.7, P > 0.05). CONCLUSION: AST and QUE might be beneficial in the protection of myocardial cells against hypoxia because of attenuation of oxidative damage. The protective effects of both AST and QUE are better than that of VitE, and that of AST is better than QUE as shown by a decrease in the amount of LDH and increase in the number of viable cells with the same dosage, but no obvious difference is shown between them in attenuating oxidative damage.