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二聚体 PSD-95 抑制对大鼠皮质撞击伤后兴奋性细胞死亡和结局的影响。

Effects of Dimeric PSD-95 Inhibition on Excitotoxic Cell Death and Outcome After Controlled Cortical Impact in Rats.

机构信息

Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Jagtvej 160, DK-2100, Copenhagen, Denmark.

The Unit for Cognitive Neuroscience (UCN), Department of Psychology, Faculty of Social Sciences, University of Copenhagen, Copenhagen, Denmark.

出版信息

Neurochem Res. 2017 Dec;42(12):3401-3413. doi: 10.1007/s11064-017-2381-y. Epub 2017 Aug 21.

DOI:10.1007/s11064-017-2381-y
PMID:28828633
Abstract

Therapeutic effects of PSD-95 inhibition have been demonstrated in numerous studies of stroke; however only few studies have assessed the effects of PSD-95 inhibitors in traumatic brain injury (TBI). As the pathophysiology of TBI partially overlaps with that of stroke, PSD-95 inhibition may also be an effective therapeutic strategy in TBI. The objectives of the present study were to assess the effects of a dimeric inhibitor of PSD-95, UCCB01-144, on excitotoxic cell death in vitro and outcome after experimental TBI in rats in vivo. In addition, the pharmacokinetic parameters of UCCB01-144 were investigated in order to assess uptake of the drug into the central nervous system of rats. After a controlled cortical impact rats were randomized to receive a single injection of either saline or two different doses of UCCB01-144 (10 or 20 mg/kg IV) immediately after injury. Spatial learning and memory were assessed in a water maze at 2 weeks post-trauma, and at 4 weeks lesion volumes were estimated. Overall, UCCB01-144 did not protect against NMDA-toxicity in neuronal cultures or experimental TBI in rats. Important factors that should be investigated further in future studies assessing the effects of PSD-95 inhibitors in TBI are discussed.

摘要

PSD-95 抑制在许多中风研究中已显示出治疗效果;然而,只有少数研究评估了 PSD-95 抑制剂在创伤性脑损伤 (TBI) 中的作用。由于 TBI 的病理生理学与中风部分重叠,PSD-95 抑制也可能是 TBI 的一种有效治疗策略。本研究的目的是评估 PSD-95 二聚体抑制剂 UCCB01-144 对体外兴奋性细胞死亡和体内实验性 TBI 后大鼠结局的影响。此外,还研究了 UCCB01-144 的药代动力学参数,以评估该药物在大鼠中枢神经系统中的摄取情况。在皮质控制冲击后,大鼠随机接受单次注射生理盐水或两种不同剂量的 UCCB01-144(10 或 20mg/kg IV),在损伤后立即注射。在创伤后 2 周,通过水迷宫评估空间学习和记忆,在 4 周时估计损伤体积。总的来说,UCCB01-144 不能预防神经元培养物中的 NMDA 毒性或大鼠实验性 TBI。在评估 PSD-95 抑制剂在 TBI 中的作用的未来研究中,还应进一步探讨一些重要因素。

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本文引用的文献

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PSD-95 uncoupling from NMDA receptors by Tat- N-dimer ameliorates neuronal depolarization in cortical spreading depression.Tat-N-二聚体使PSD-95与NMDA受体解偶联可改善皮层扩散性抑制中的神经元去极化。
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普雷索通过调节创伤性脑损伤后一氧化氮和钙反应来调节 NMDA 受体介导的兴奋性毒性。
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