中文摘要：

背景服的 ischemia-reperfusion 损害是为在 ischemic 的神经原的损失的主要原因脑血管的疾病。因此，深深地理解它的致病并且发现一个新目标是要解决的关键问题。这研究试图调查对氧葡萄糖 deprivation/reperfusion (OGD/RP ) 的 salvianolic 酸 B (SalB ) 的效果在主要老鼠损坏的 neuroprotective 外皮的 neurons.Methods 新生的威斯特老鼠的主要文化随机被划分成控制组， OGD/RP 组和 SalB 处理组(10 mg/L ) 。房间模型被分别地剥夺氧和葡萄糖 3 个小时和灌注 3 个小时和 24 个小时建立。神经原生存能力被 MTT 试金决定。细胞的反应的氧种类(ROS ) 的水平被荧光灯的标记检测方法和纺纱套住技术分别地。neuronal Mn-superoxide dismutase (Mn 草皮) 的活动，过氧化氢酶(猫) 和谷胱甘肽 peroxidase (GSH-PX ) 是由 chromatometry 的 assayed。线粒体膜潜力(m) 是流动 cytometry 分析的份量上。细胞色素 c 的版本率被西方的弄污检测。neuronal 超微结构被传播电子显微镜学观察。统计意义被 Student-Newman-Keuls test.Results OGD/RP 跟随的变化(ANOVA ) 的分析评估增加了细胞的 ROS 的水平，但是减少房间生存能力和 Mn 草皮，猫和 GSH-PX 的活动；SalB 处理显著地减少了 ROS (P 0.05 ) 的水平；并且提高了房间生存能力(P 0.05 ) 和这些 antioxidases (P 0.05 ) 的活动。另外， OGD/RP 导致了 m 的荧光价值减少并且到上升的细胞色素 c 的版本率尤其是；SalB 显著地提高了 m (P 0.01 ) 的水平并且压抑细胞色素 c (P 0.05 ) 的版本率；它也改善了 neuronal 词法 injury.Conclusion SalB 的 neuroprotection 可以被归因于 ROS 的消除和 apoptosis 的抑制。

英文摘要：

Background Cerebral ischemia-reperfusion injury is the main reason for the loss of neurons in the ischemic cerebrovascular disease. Therefore, to deeply understand its pathogenesis and find a new target is the key issue to be solved. This research aimed to investigate the neuroprotective effects of salvianolic acid B （SalB） against oxygen-glucose deprivation/reperfusion （OGD/RP） damage in primary rat cortical neurons.Methods The primary cultures of neonatal Wister rats were randomly divided into the control group, the OGD/RP group and the SalB-treatment group （10 mg/L）. The cell model was established by depriving of oxygen and glucose for 3 hours and reperfusion for 3 hours and 24 hours, respectively. The neuron viability was determined by MTT assay. The level of cellular reactive oxygen species （ROS） was detected by fluorescent labeling method and spin trapping technique respectively. The activities of neuronal Mn-superoxide dismutase （Mn-SOD）, catalase （CAT） and glutathione peroxidase （GSH-PX） were assayed by chromatometry. The mitochondria membrane potential （△ψm） was quantitatively analyzed by flow cytometry. The release rate of cytochrome c was detected by Western blotting. The neuronal ultrastructure was observed by transmission electron microscopy. Statistical significance was evaluated by analysis of variance （ANOVA）followed by Student-Newman-Keuls test.Results OGD/RP increased the level of cellular ROS, but decreased the cell viability and the activities of Mn-SOD, CAT and GSH-PX; SalB treatment significantly reduced the level of ROS （P ＜0.05）; and enhanced the cell viability （P ＜0.05）and the activities of these antioxidases （P ＜0.05）. Additionally, OGD/RP induced the fluorescence value of △ψm to diminish and the release rate of cytochrome c to rise notably; SalB markedly elevated the level of △ψm （P ＜0.01） and depressed the release rate of cytochrome c （P ＜0.05）; it also ameliorated the neuronal morphological injury.Conclusion Th