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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Effects of Memantine on Nitric Oxide Production and Hydroxyl Radical Metabolism during Cerebral Ischemia and Reperfusion in Mice
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Effects of Memantine on Nitric Oxide Production and Hydroxyl Radical Metabolism during Cerebral Ischemia and Reperfusion in Mice

机译：念珠内对小鼠脑缺血和再灌注中的一氧化氮产生和羟基自由基代谢的影响

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Background: The purpose of this study was to investigate the effects of memantine on brain ischemia. Because we can measure nitric oxide (NO) production and hydroxyl radical metabolism continuously, we investigated the effect of memantine on NO production and hydroxyl radical metabolism in cerebral ischemia and reperfusion. Methods: Memantine (25 mu mol/kg) was administered intraperitoneally to 6 C57BL/6 mice 30 minutes before ischemia. Seven additional mice received no injection (controls). NO production and hydroxyl radical metabolism were continuously monitored using bilateral striatal microdialysis in vivo. Hydroxyl radical formation was monitored using the salicylate trapping method. Forebrain ischemia was produced in all mice by occluding the common carotid artery bilaterally for 10 minutes. Levels of the NO metabolites nitrite (NO2-) and nitrate (NO3-) were determined using the Griess reaction. Survival rates of hippocampal CA1 neurons were calculated and 8-hydroxydeoxyguanosine (8-OHdG)-immunopositive cells were counted to evaluate the oxidative stress in hippocampal CA1 neurons 72 hours after the start of reperfusion. Results: The regional cerebral blood flow was significantly higher in the memantine group than in the control group after reperfusion. Furthermore, the level of 2,3-dihydroxybenzoic acid was significantly lower in the memantine group than in the control group during ischemia and reperfusion. Levels of NO2- and NO3- did not differ significantly between the 2 groups. Although survival rates in the CA1 did not differ significantly, there were fewer 8-OHdG-immunopositive cells in animals that had received memantine than in control animals. Conclusions: These data suggest that memantine exerts partially neuroprotective effects against cerebral ischemic injury.
机译：背景：本研究的目的是探讨Memantine对脑缺血的影响。因为我们可以连续测量一氧化氮（NO）生产和羟基自由基代谢，我们研究了Memantine对脑缺血和再灌注中没有生产和羟基自由基代谢的影响。方法：在缺血前30分钟腹膜内施用Memantine（25μmol/ kg）至6c57bl / 6小鼠。七只额外小鼠没有注射（对照）。在体内使用双侧纹纹体微岩不断监测没有生产和羟基自由基代谢。使用水杨酸盐捕获方法监测羟基自由基。通过封闭常见的颈动脉10分钟，在所有小鼠中产生前脑缺血。使用GRIESS反应测定NO Idabolites亚硝酸盐（NO 2-）和硝酸盐（NO 3-）的水平。计算海马CA1神经元的存活率，计数8-羟基氧杂核苷酸（8-OHDG） - 免疫阳性细胞，以在再灌注开始后72小时评价海马CA1神经元中的氧化应激。结果：在再灌注后，Memantisine组的区域脑血流量显着高于对照组。此外，在缺血再灌注过程中，在Memantine组中的2,3-二羟基苯甲酸的水平显着低于对照组。 2组之间的NO2和NO3的水平没有显着差异。虽然CA1中的存活率没有显着差异，但是在对照动物中获得了Memantine的动物中的8-OHDG-Immunyive细胞较少。结论：这些数据表明，Memantine施加部分神经保护作用对脑缺血性损伤。

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