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17β雌二醇对氯胺酮诱导皮层神经元凋亡的影响

李建立 高冬艳 杜彦茹 侯艳宁

中国药理学通报Issue(6):816-820,5.
中国药理学通报Issue(6):816-820,5.DOI:10.3969/j.issn.1001-1978.2014.06.017

17β雌二醇对氯胺酮诱导皮层神经元凋亡的影响

17β-estradiol protects cortical neurons from ketamine-induced apoptosis

李建立 1高冬艳 1杜彦茹 1侯艳宁2

作者信息

  • 1. 河北省人民医院麻醉科,河北 石家庄 050051
  • 2. 白求恩国际和平医院药剂科,河北 石家庄 050082
  • 折叠

摘要

Abstract

Aim To investigate the effects of 17β-es-tradiol on the apoptosis induced by ketamine in primary cultured cortical neurons. Methods Primary cultured cortical neurons were treated with different concentra-tions of ketamine or 17β-estradiol respectively. 24 hours after various treatments, neuron viability was measured by MTT assay. The structure of neurons was analyzed using microscope. Apoptotic neurons were de-termined by the TUNEL assay. The level of pAkt ex-pression was analyzed by Western blot. ResultsCompared with the control group, ketamine decreased neuron viability in a dose-dependent manner. Com-pared with ketamine group, 17β-estradiol increased neuron viability in a dose-dependent manner. Lack of three-dimensional sense,faded color,uncleared outline <br> were observed, and fractured neuron axons or neurons death were also observed in neurons treated by 100μmol · L-1 ketamine. 100 μmol · L-1 ketamine in-creased the number of apoptotic neurons and decreased the expression of pAkt. 0.1 μmol · L-1 17β-estradiol decreased the number of apoptotic neurons and in-creased the expression of pAkt. LY294002 inhibited the protective effects of 17β-estradiol, the number of apoptotic neurons increased, and the level of pAkt de-creased significantly. Conclusion 17β-estradiol ex-erts the neuroprotective effects against ketamine-in-duced neuroapoptosis by activating the PI3 K/Akt sig-naling pathway.

关键词

17β雌二醇/氯胺酮/皮层神经元/凋亡/Akt/LY294002/神经保护

Key words

17β-estradiol/ketamine/cortical neu-rons/apoptosis/Akt/LY294002/neuroprotection

分类

医药卫生

引用本文复制引用

李建立,高冬艳,杜彦茹,侯艳宁..17β雌二醇对氯胺酮诱导皮层神经元凋亡的影响[J].中国药理学通报,2014,(6):816-820,5.

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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