ogd

Conclusions We have established a simple , stable and reliable modle of OGD / R of vascular endothelial cells in vitro successfully .

结论：（1）建立了一种简便、稳定和可靠的体外血管内皮细胞氧糖剥夺/复氧模型；

OGD preconditioning could lighten the changes of tight junction proteins ZO-1 and F-actin location . 3 .

氧糖剥夺预处理可使脑微血管内皮细胞紧密连接相关蛋白ZO-1和细胞骨架蛋白F-actin的位置改变减轻。

RESULTS : ① Cell survival rate decreased with OGD duration .

结果：①随着氧/葡萄糖剥夺时间延长，神经细胞存活率下降。

So another batch of neuronal supplemental measure was applied to test normal group and OGD group .

所以接下来利用另外一批次的神经元补充测量正常组和糖氧剥夺组。

Bradykinin B1 receptor can increase neuron apoptosis induced by OGD .

研究提示：1、B1受体可以增加OGD所致的神经元凋亡。

Fetal rat cortical neurons were cultured as chapter one , OGD and hypothermia phase as chapter two .

本章按照第一章方法原代培养胎鼠皮层神经元，然后按照第二章的方法制作糖氧剥夺模型以及实施低温干预。

Conclusion The neuronal injury induced by OGD is partly mediated by the mitochondrial apoptosis pathway ;

结论①缺血再灌注引起的神经元凋亡部分是通过线粒体凋亡途径；

Methods An ischemic model was developed in PC12 cell line with treatment of oxygen glucose deprivation ( OGD ) .

方法采用氧葡萄糖剥夺（OGD）方法在PC12细胞上建立缺血模型。

Changes of GluRs on postsynaptic membrane and delayed neuron death after OGD

OGD后突触后膜GluRs含量变化及神经元延迟性死亡研究

Cell fluorescence intensity of OGD group and AOAA + OGD group was significantly decreased compared with that of control group .

OGD组和AOAA+OGD组的细胞荧光强度较对照组明显减弱。

Conclusion : GM1 could protect injury induced by OGD / Rep in rat hippocampal slices effectively in vitro .

结论：GM1可以有效的保护体外大鼠海马脑片缺糖/缺氧再灌注损伤。

After OGD 12h , the activity of astrocytes descend gradually along with the time of reoxygenation .

星形胶质细胞在糖氧剥夺12小时后再复糖复氧时，随着复氧时间的延续，其活性持续下降。

Neurons were assigned randomly into control group , hypoxia group , OGD group , MK-801 group and d-APV group .

将神经细胞随机分为正常对照组、单纯缺氧组、无糖缺氧组、MK-801组和d-APV组。

Methods In vitro ischemic injury of hippocampal slices was induced by oxygen-glucose deprivation ( OGD ) .

方法大鼠海马脑片以缺氧缺糖（OGD）诱导缺血损伤后，实时检测CA1区透光度变化评价细胞水肿；

Acidosis induced neuronal damage during both OGD and reperfusion . However , it caused more detrimental injury during reperfusion .

实验发现，OGD和再灌注过程中，酸中毒均引起了神经元的损伤，然而与OGD相比，再灌注过程中酸中毒损伤显著加剧。

Observation of the effect of minocycline on light transmittance change induced by OGD or NMDA in rat hippocampal slices .

米诺环素对海马脑片OGD及NMDA损伤的作用：OGD损伤使海马脑片放射层透光度（LT）显著增加；MK一801（l抖mol/L）可显著抑制OGD引起的LT峰值增高（尸<0.05）；

Objective : To make a convenient and practical in vitro ischemia model by oxygen and glucose deprivation ( OGD ) in cultured neuronal cells .

目的：探讨建立一种方便、实用的神经细胞离体氧、糖剥夺体外缺血模型。

Objective To investigate the role of HPK1 in hippocampus neuron apoptosis induced by oxygen-glucose deprivation ( OGD ) .

研究了达曲班对体外培养心肌细胞缺氧缺糖性损伤的保护作用。

DAPI staining was used to investigate the role of HPK1 antisense oligodeoxynucleotides in hippocampus neuron death induced by OGD .

采用DAPI染色技术观察HPK1反义寡核苷酸对OGD诱导的海马神经元凋亡的作用。

The in vitro ischemic injury was induced by oxygen-glucose deprivation ( OGD ) for 1.5 h and reperfusion for 24 h.

以缺氧缺糖（oxygen-glucosedeprivation，OGD）1.5h和再灌24h诱导神经元损伤。

Conclusion Baicalin possesses protective effect on OGD injury in rat brain slices , which is related to its inhibitory effect on excitatory amino acids toxicity .

结论黄芩苷对大鼠脑片缺氧缺糖性损伤具有一定的保护作用，作用机制可能与其抑制了兴奋性氨基酸毒性有关。

Objective To understand the protective effect and possible mechanism of Lig on cultured rat astrocytes in oxygen-glucose deprivation ( OGD ) in vitro .

目的探讨川芎嗪对离体大鼠星形胶质细胞在糖氧剥离损伤中的作用及可能机制。

LDH release were significantly increased in OGD and IHB groups compared with that in HBO group , Sham group and ACT group ( p0.05 ) .

OGD后24h，OGD组、IHB组、HBO组和Sham组与ACT组相比，LDH释放量明显增多（P0.05）。

Objective To investigate the protective effects of hyperoxia solution ( HS ) on the oxygen and glucose deprivation ( OGD ) in cultured neuronal cells .

目的观察高氧液对氧糖剥夺（OGD）离体神经元损伤的保护作用。

Objective : To establish a simple , sensitive in vitro method to evaluate oxygen / glucose deprivation ( OGD ) induced injury of brain hippocampal slices in rats .

目的：建立一种定量评价离体脑片缺糖/缺氧损伤的简便、快速、灵敏的方法。

Methods SD rat cerebellar granule cells were isolated and cultured , and mimic ischemia-reperfusion model was established by oxygen-glucose-deprivation ( OGD ) in vitro .

方法用原代培养的SD乳鼠小脑颗粒细胞建立以缺氧缺糖模拟缺血再灌注模型，并加不同浓度的MT（10-5、10-7、10-9mol/L）孵育。

CONCLUSION : Pretreatment of Gin B and HP have protective effects on astrocytes after OGD 24 hours , which is related to the improvement of expression of EPO .

结论：银杏内酯B与低氧预适应对氧-葡萄糖剥夺星形胶质细胞有保护作用，其作用发生可能与促进促红细胞生成素表达有关。

After OGD and H2O2 treatments , GFP / 5-LOX was translocated to the nuclear membrane in 50.6 % and 57.7 % cells respectively .

OGD和H2O2处理后，分别有50.6%和57.7%细胞的GFP/5-LOX移位到核膜；

Objective ( 1 ) To establish a simple , stable and reliable modle of oxygen glucose deprivation / reoxygenation ( OGD / R ) of vascular endothelial cells in vitro .

目的：（1）建立一种方便、稳定、可靠的体外细胞氧糖剥夺（OxygenGlucoseDeprivation，OGD）／复氧（reoxygenation）模型；

The protective effect of ketamine was also evaluated . Results : Both intensity and area of cortex and striatum TTC staining were significantly reduced after 7.5 ~ 15 min of OGD .

结果：纹状体和皮层TTC染色平均灰度和面积随OGD时间的延长而下降，在7.5～15min时明显下降；