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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Preconditioning with sublethal ischemia or intermittent normobaric hyperoxia up-regulates glutamate transporters and tumor necrosis factor-alpha converting enzyme in the rat brain.
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Preconditioning with sublethal ischemia or intermittent normobaric hyperoxia up-regulates glutamate transporters and tumor necrosis factor-alpha converting enzyme in the rat brain.

机译：致死性局部缺血或间歇性常压高氧预处理可以上调大鼠脑中的谷氨酸转运蛋白和肿瘤坏死因子-α转化酶。

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INTRODUCTION: Recent studies suggest that sublethal ischemia and intermittent normobaric hyperoxia (InHO) protect the brain from subsequent ischemic injury. In this, changes in the expression of excitatory amino-acid transporters (EAATs) and tumor necrosis factor-alpha converting enzyme (TACE) may play a role. We sought to identify and clarify the nature of any such changes. METHOD: Rats were divided into 3 experimental groups, each of 15 animals. The first group was exposed to normobaric hyperoxia (fractional inspired oxygen concentration 95%) for 4 hours/day for 6 consecutive days (InHO). The second group acted as controls, and was exposed to 21% oxygen in the same chamber (room air). The third group acted as a model of ischemic preconditioning, and was exposed to 21% oxygen in the same chamber and subjected to 10 minutes of temporary middle cerebral artery (MCA) occlusion (tMCAO). After 24 hours, 9 animals from each group were subjected to 60 minutes of right MCA occlusion (MCAO). After 24 hours of reperfusion, neurologic deficit score and infarct volume were assessed in MCAO-operated subgroups. The remaining 6 animals in each group remained intact and, 48 hours after pretreatment, were killed for assessment of EAATs and TACE expression in the ipsilateral hemisphere. RESULTS: Preconditioning with InHO and tMCAO decreased neurologic deficit score and infarct volume, and increased expression of EAAT1, EAAT2, EAAT3, and TACE. CONCLUSION: InHO and tMCAO are associated with expression of EAAT1, EAAT2, EAAT3, and TACE, consistent with an active role in the genesis of ischemic protection.
机译：引言：最近的研究表明，致死性局部缺血和间歇性常压高氧血症（InHO）可保护大脑免受随后的缺血性损伤。在这种情况下，兴奋性氨基酸转运蛋白（EAAT）和肿瘤坏死因子-α转化酶（TACE）的表达变化可能起作用。我们试图确定并澄清任何此类更改的性质。方法：将大鼠分为3组，每组15只。第一组连续6天（InHO）暴露于常压高氧症（分数吸氧浓度为95％）每天4小时。第二组作为对照，并在同一室内（室内空气）中暴露于21％的氧气。第三组充当缺血预处理的模型，并在同一腔室中暴露于21％的氧气，并经过10分钟的临时性大脑中动脉（MCA）阻塞（tMCAO）。 24小时后，将每组的9只动物进行60分钟的右MCA闭塞（MCAO）。再灌注24小时后，评估MCAO手术亚组的神经功能缺损评分和梗塞体积。每组中其余6只动物保持完整，并在预处理后48小时处死，以评估同侧半球中的EAAT和TACE表达。结果：用InHO和tMCAO进行预处理可降低神经功能缺损评分和梗塞体积，并增加EAAT1，EAAT2，EAAT3和TACE的表达。结论：InHO和tMCAO与EAAT1，EAAT2，EAAT3和TACE的表达有关，与缺血保护的起因有关。

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