首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Involvement of Glutamate Transporter-1 in Neuroprotection against Global Brain Ischemia-Reperfusion Injury Induced by Postconditioning in Rats
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Involvement of Glutamate Transporter-1 in Neuroprotection against Global Brain Ischemia-Reperfusion Injury Induced by Postconditioning in Rats

机译:谷氨酸转运蛋白-1参与对大鼠后处理引起的全脑缺血再灌注损伤的神经保护作用

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摘要

Ischemic postconditioning refers to several transient reperfusion and ischemia cycles after an ischemic event and before a long duration of reperfusion. The procedure produces neuroprotective effects. The mechanisms underlying these neuroprotective effects are poorly understood. In this study, we found that most neurons in the CA1 region died after 10 minutes of ischemia and is followed by 72 hours of reperfusion. However, brain ischemic postconditioning (six cycles of 10 s/10 s reperfusion/re-occlusion) significantly reduced neuronal death. Significant up-regulation of Glutamate transporter-1 was found after 3, 6, 24, 72 hours of reperfusion. The present study showed that ischemic postconditioning decreases cell death and that upregulation of GLT-1 expression may play an important role on this effect.
机译:缺血后处理是指在缺血事件之后和长时间再灌注之前的几个短暂的再灌注和缺血周期。该过程产生神经保护作用。这些神经保护作用的潜在机制了解甚少。在这项研究中,我们发现CA1区的大多数神经元在缺血10分钟后死亡,然后再灌注72小时。但是,脑缺血后处理(六个周期的10 s / 10 s再灌注/重新阻塞)显着降低了神经元死亡。再灌注3、6、24、72小时后,发现谷氨酸转运蛋白1明显上调。本研究表明,缺血后处理可减少细胞死亡,而GLT-1表达的上调可能在此作用中起重要作用。

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