Estradiol after cardiac arrest and cardiopulmonary resuscitation is neuroprotective and mediated through estrogen receptor-beta.
Estradiol after cardiac arrest and cardiopulmonary resuscitation is neuroprotective and mediated through estrogen receptor-beta.
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心脏骤停和心肺复苏后的雌二醇具有神经保护作用，并通过雌激素受体β介导。
DOI：
10.1038/jcbfm.2008.116
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发表时间：
2009-02
期刊：
影响因子：
--
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我们评估了心脏骤停和心肺复苏（CA/CPR）后长期给予雌激素对神经组织病理学和行为学结果的影响。我们还研究了使用ER-α激动剂丙基吡唑三醇（PPT）和ER-β激动剂二芳基丙腈（DPN）刺激雌激素受体（ER）对CA/CPR后神经元存活的影响，以确定雌激素的神经保护作用是否可能是ER介导的。雄性C57 B1/6小鼠经历10分钟CA/CPR和3天存活。在方案1中，根据治疗组，静脉注射溶剂（NaCl 0.9%）和0.5或2.5 µg 17β-雌二醇（E2负荷剂量），然后皮下植入含溶剂（油）或E2（12.6 µg）的皮下植入物。在实验方案2中，给小鼠注射（静脉内）ER-α激动剂PPT或ER-β激动剂DPN，然后皮下注射含有PPT（200 µg）或DPN（800 µg）的Alzet泵植入物。长期给予E2可减少任一负荷剂量给药后纹状体神经元的损伤（41% ± 19%，35% ± 26%的损伤神经元），与赋形剂（68% ± 7%，P< 0.01）相比，对海马CA 1区无影响。在方案2中，与ER-α激动剂PPT（68% ± 10%）和赋形剂（69% ± 11%; P < 0.01）相比，ER-β激动剂DPN治疗减少纹状体中的神经元损伤（51% ± 13%损伤的神经元）。雌激素β受体激动剂DPN可减轻海马CA 1区神经元损伤（29% ± 22%），而雌激素α受体激动剂PPT则可减轻损伤（62% ± 33%），差异有统计学意义（P < 0.05）。溶剂组和ER-α激动剂组动物的海马CA 1区损伤无差异。我们得出结论，CA/CPR后长期给予E2具有神经保护作用，这种作用最有可能通过ER-β介导。
We evaluated long-term administration of estrogen after cardiac arrest and cardiopulmonary resuscitation (CA/CPR) on neurohistopathological and behavioral outcome. We also examined the effect of estrogen receptor (ER) stimulation using ER-α agonist propyl pyrazole triol (PPT) and ER-β agonist diarylpropionitrile (DPN) on neuronal survival after CA/CPR to determine whether possible neuroprotective effects of estrogen are ER-mediated. Male C57Bl/6 mice underwent 10 mins of CA/CPR and 3-day survival. In protocol 1, intravenous injection of vehicle (NaCl 0.9%) and 0.5 or 2.5 µg 17β-estradiol (E2 loading dose) was performed followed by subcutaneous implants containing vehicle (oil) or E2 (12.6 µg), according to a treatment group. In experimental protocol 2, mice were injected (intravenously) with the ER-α agonist PPT or ER-β agonist DPN followed by Alzet pump implants (subcutaneously) containing PPT (200 µg) or DPN (800 µg). Long-term E2 administration reduced neuronal injury in the striatum after administration of either loading dose (41% ± 19%, 35% ± 26% of injured neurons), as compared with vehicle (68% ± 7%, P< 0.01), with no effect in the hippocampal CA1 field. In protocol 2, treatment with ER-β agonist DPN reduced neuronal injury in the striatum (51% ± 13% injured neurons) as compared with ER-α agonist PPT (68% ± 10%) and vehicle (69% ± 11%; P < 0.01). Estrogen receptor-β agonist DPN reduced neuronal injury in the hippocampal CA1 field (29% ± 22% injured neurons) as compared with ER-α agonist PPT treatment (62% ± 33%; P < 0.05). Injury was not different in hippocampal CA1 between vehicle and ER-α agonist-treated animals. We conclude that long-term E2 administration after CA/CPR is neuro-protective and that this effect is most likely mediated via ER-β.
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影响因子：
120.7
作者：
Cobb, LA;Fahrenbruch, CE;Hallstrom, AP
通讯作者：
Hallstrom, AP
影响因子：
3
作者：
Kofler, J;Hattori, K;Traystman, RJ
通讯作者：
Traystman, RJ
影响因子：
6.5
作者：
Herlitz, J;Rundqvist, S;Lindkvist, J
通讯作者：
Lindkvist, J
DOI：
10.1016/s0169-328x(98)00298-8
发表时间：
1999-03-05
期刊：
MOLECULAR BRAIN RESEARCH
影响因子：
--
作者：
Böttiger, BW;Teschendorf, P;Gass, P
通讯作者：
Gass, P
影响因子：
2.5
作者：
Küppers, E;Beyer, C
通讯作者：
Beyer, C