右美托咪定对高浓度氧引起的新生大鼠脑损伤的保护作用
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Neuroprotective effects of dexmedetomidine against hyperoxia-induced injury in the developing rat brain
背景与目的
右美托咪定（DEX）是一种高选择性激动剂α2 -受体，具有镇静、镇痛、抗焦虑作用。右美托咪定在各种脑损伤模型中的神经保护作用已有报道。本研究探讨右旋美托咪啶对海马神经形成的影响，尤其是高氧诱导后新生大鼠神经元的增殖、成熟和神经元可塑性
方 法
6日龄性别配对Wistar大鼠分别暴露于80% O2或室内空气24小时，并用右旋美托咪啶（1, 5或10μg/kg）或生理盐水进行处理。
结 果
单次右美托咪定预处理减弱高浓度氧引起的神经发生和可塑性方面的损伤。具体来说，与对照组相比，高浓度氧组其增殖能力（(PCNA+细胞）及神经元标记物的表达量（Nestin+, PSA-NCAM+, NeuN+ cells）和转录因子（SOX2, Tbr1/2, Prox1）显著减少。此外，神经元可塑性调节因子（(Nrp1, Nrg1, Syp, 和 Sema3a/f）也呈现急剧下降。与高浓度组相比，高浓度氧暴露前右美托咪啶的单次给药导致表达谱的显著上调。
结 论
我们的研究结果表明，右美托咪定可能对新生大鼠急性高浓度氧模型的具有神经保护作用。
原始文献摘要
Endesfelder S1, Makki H1, von Haefen C2 PLoS One. 2017 Feb 3;12(2):e0171498. doi: 10.1371/journal.pone.0171498. eCollection 2017.
Abstract
Dexmedetomidine (DEX) is a highly selective agonist of α2-receptors with sedative, anxiolytic, and analgesic properties. Neuroprotective effects of dexmedetomidine have been reported in various brain injury models. In the present study, we investigated the effects of dexmedetomidine on hippocampal neurogenesis, specifically the proliferation capacity and maturation of neurons and neuronal plasticity following the induction of hyperoxia in neonatal rats. Six-day old sex-matched Wistar rats were exposed to 80% oxygen or room air for 24 h and treated with 1, 5 or 10 μg/kg of dexmedetomidine or normal saline. A single pretreatment with DEX attenuated the hyperoxia-induced injury in terms of neurogenesis and plasticity. In detail, both the proliferation capacity (PCNA+ cells) as well as the expression of neuronal markers (Nestin+, PSA-NCAM+, NeuN+ cells) and transcription factors (SOX2, Tbr1/2, Prox1) were significantly reduced under hyperoxia compared to control. Furthermore, regulators of neuronal plasticity (Nrp1, Nrg1, Syp, and Sema3a/f) were also drastically decreased. A single administration of dexmedetomidine prior to oxygen exposure resulted in a significant up-regulation of expression-profiles compared to hyperoxia. Our results suggest that dexmedetomidine may have neuroprotective effects in an acute hyperoxic model of the neonatal rat.
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