Excitotoxicity is one of the main mechanisms related to hypoxia/reoxygenation (H/R) injury. Excitatory amino acid transporter (EAAT)2 mainly distributes on astrocytes and plays an important role on glutamate reuptake and glutamate homeostasis. Midazolam has a neuroprotective effect in some neuropathological conditions. The present study aimed to detect the role of EAAT2 in the neuroprotective effect of midazolam in neonatal rat brain subjected to H/R. Pretreatment with midazolam reversed H/R-induced apoptosis and downregulation of EAAT2 mRNA and protein expression in the hippocampus. Pretreatment with dihydrokainic acid (a selective inhibitor of EAAT2) exacerbated apoptosis, and thus inhibited the neuroprotective effect of midazolam against H/R injury. We demonstrated for the first time that dysregulation of EAAT2 expression may be related to the neural injury induced by H/R in rat pups, and pretreatment with midazolam attenuated apoptosis and improved learning and memory partly due to regulating EAAT2 expression.

中文翻译：

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咪达唑仑通过调节 EAAT2 有助于对新生大鼠缺氧/复氧诱导的脑损伤的神经保护作用。

兴奋性毒性是与缺氧/复氧 (H/R) 损伤相关的主要机制之一。兴奋性氨基酸转运蛋白 (EAAT)2 主要分布于星形胶质细胞，对谷氨酸再摄取和谷氨酸稳态起重要作用。咪达唑仑在某些神经病理学病症中具有神经保护作用。本研究旨在检测 EAAT2 在咪达唑仑对 H/R 新生大鼠脑神经保护作用中的作用。咪达唑仑预处理可逆转 H/R 诱导的海马细胞凋亡和 EAAT2 mRNA 和蛋白质表达的下调。用二氢红藻氨酸（EAAT2 的选择性抑制剂）预处理会加剧细胞凋亡，从而抑制咪达唑仑对 H/R 损伤的神经保护作用。