中文摘要：

目的探讨当归红芪多糖对辐射损伤氧化应激诱导的心肌细胞线粒体凋亡通路异常的影响。方法原代培养Wistar大鼠乳鼠心肌细胞,X线照射心肌细胞建立辐射损伤模型,用不同浓度的当归红芪多糖进行干预。实验分正常对照组、辐射损伤模型组（照射剂量为6 Gy）、当归红芪多糖低剂量组（终浓度为25 mg/L）、当归红芪多糖中剂量组（终浓度为50 mg/L）、当归红芪多糖高剂量组（终浓度为100 mg/L）。MTT法检测各组心肌细胞生长抑制率;DCFH-DA荧光探针检测各组心肌细胞活性氧自由基（ROS）表达水平;激光共聚焦技术检测各组心肌细胞线粒体膜电位水平;蛋白印迹法检测各组心肌细胞内细胞色素C（Cyt C）、Caspase-3、Caspase-9蛋白的相对表达量。结果与正常对照组相比,辐射损伤组心肌细胞生长抑制率明显升高、线粒体膜电位降低、ROS表达及Cyt C、Caspase-3、Caspase-9蛋白的相对表达量明显升高,差异具有显著性（P〈0.05）。与辐射损伤组相比,当归红芪多糖各干预组心肌细胞生长抑制率均不同程度下降、线粒体膜电位有所升高、ROS表达及Cyt C、Caspase-3、Caspase-9蛋白的相对表达量均不同程度降低（P〈0.05）。结论辐射致心肌细胞凋亡的机制之一是线粒体凋亡通路的激活,当归红芪多糖通过调控该通路发挥心肌细胞保护作用。

英文摘要：

Objective To investigate the effects of polysaccharide in angelica（ Danggui,Radix Angelicae Sinensis） and hedysari（ Hongqi,Radix Hedysari） combination on the pathway of mitochondrial apoptosis caused by radiation injury induced oxidative stress in myocardial cells of neonatal rats. Method Myocardial cells of Wistar neonatal rats were obtained from in vitro primary culture and radiation injury model was established by using direct X-ray exposure. Different concentrations of angelica and hedysari polysaccharide were administered as intervention. Cells were randomly divided into five groups： normal control group,radiation injury model group（ 5Gy exposure dose）,low-dose polysaccharide intervention group（ 25 mg / L,DGHQ-L group）,mid-dose polysaccharide intervention group（ 50 mg / L,DGHQ-M group）,and high-dose polysaccharide intervention group（ 100 mg / L,DGHQ-H group）. Growth inhibition rates of cells were measured with tetrazolium（ MTT） Colorimetric assay while levels of reactive oxygen species（ ROS） were assessed with fluorescent probe DCFH-DA. Mitochondrial membrane potential was measured with confocal scanning laser microscopy and expression levels of cytochrome C（ Cyt C）,caspases-3,and caspases-9 were detected with Western blot assay. Results Compared with the normal control group,growth inhibition rate of rat myocardial cells in the radiation injury model group was significantly increased,with a marked decrease in mitochondrial potential（ ΔΨm） and a significant elevation in the expression levels of ROS,Cyt C,caspases-3,and caspases-9（ P〈0. 05） in the model group as well. Compared with the model group,growth inhibition rates of rat myocardial cells were significantly decreased in all DGHQ groups. Mitochondrial potential（ ΔΨm） increased while the expression levels of ROS,Cyt C,caspases-3,and caspases-9decreased（ P〈0. 05）. Conclusion The activation of mitochondrial apoptosis pathway is one of the main mechanism of myocardial cell apoptosis induced by X r