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作 者:黄海霞[1] 莫晓燕[1] 杜晓阳[2] 张振强[2] 耿涛[2]
机构地区:[1]西安交通大学生命科学与技术学院,陕西西安710049 [2]西安交通大学医学院,陕西西安710061
出 处:《时珍国医国药》2005年第10期963-965,共3页Lishizhen Medicine and Materia Medica Research
基 金:陕西省西安市工业科技资助项目(No.GG040661)
摘 要:目的:通过建立心肌损伤模型探讨赤芍总苷对培养乳鼠心肌细胞损伤后细胞凋亡的影响。方法:以异丙基肾上腺素加入培养乳鼠心肌细胞造成缺血缺氧损伤模型,对比分析正常组、不同剂量赤芍总苷组和辅酶Q10阳性对照组的细胞形态学以及心肌细胞凋亡等角度探讨赤芍总苷对损伤心肌细胞保护作用的机理及其有效剂量,为中药有效成分治疗心血管疾病提供实验及理论依据。结果:损伤组细胞搏动加速,存活率下降,显示出明显的DNA凋亡特征;而辅酶Q10组和赤芍总苷组上述指标都有不同程度的改善,其中高剂量赤芍总苷组的保护作用优于阳性对照组。结论:赤芍总苷对异丙基肾上腺素造成的心肌损伤具有保护作用,并且呈现剂量依赖关系,作用机理与改善心肌缺血缺氧状态,维持细胞正常的能量代谢和收缩功能,抑制细胞凋亡有关。Objective: To investigate the influence of total paeony glycoside (TPG) on the apoptosis of cultured neonatal rat cardiomyocytes injured by developing the injured model. Methods: The ischemia and hypoxia injured model of cultured neonatal rat cardiomyocytes was induced by isoprenaline (ISO). The cell morphology and apoptosis in normal control group, different dosage TPG groups and coenzyme Q10(CoQ10) positive control group were respectively analyzed and compared. The protective mechanism and effective doses of TPG on the injured myocardial cell were investigated from the angles of biochemistry and molecular biology. The study provides both experimental and theoretical bases for the treatment of cardiovascular disease by the effective compositions of TCM. Results: Compared with normal control group, injured myocardial cells wrinkled and the frequency of beating accelerated and the survival rate of myocardial cells decreased obviously, and the DNA in injured group had obvious apoptotic phenomenon; but in TPG and CoQ10 groups all of detective indexes had improvement in varying degrees, especially high-dose TPG group in that the protective effect was better than or closed to positive control group. Conclusion: TPG has notable protective action to injured cardiomyocytes caused by ISO, which shows the relationship to dose-dependence. The functional mechanism of TPG relates to the improvement of myocardial ischemia and hypoxia, can improve the survival rate of myocardial cells, maintain normal energy metabolism and systolic function, restrain the appearance of apoptosis.
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