右美托咪定对大鼠神经元缺氧无糖损伤保护作用的实验研究

李红英; 张建杏; 王研; 于卫; 周国斌

doi:10.13418/j.issn.1001-165x.2014.04.020

中国临床解剖学杂志 ›› 2014, Vol. 32 ›› Issue (4) : 455-457. DOI: 10.13418/j.issn.1001-165x.2014.04.020

实验研究

右美托咪定对大鼠神经元缺氧无糖损伤保护作用的实验研究

李红英，　张建杏，　王研，　于卫，　周国斌

作者信息 +

Protection and mechanism of dexmedetomidine preconditioning against neuronal injury related to oxygen-glucose deprivation

LI Hong-ying, ZHANG Jian-xing, WANG Yan, YU Wei, ZHOU Guo-bin

Author information +

文章历史 +

摘要

目的　研究a2肾上腺素受体激动剂右美托咪定(dexmedetomidine，DEX)对原代培养的大鼠皮层神经元缺氧无糖损伤（OGD）的保护作用并探讨其机制。方法　建立原代培养的大鼠皮层神经元缺氧无糖损伤（OGD）模型，通过采用MTT、LDH等方法观察右美托咪定对于神经元缺氧无糖损伤的保护作用，Western blot 检测p38MAPK蛋白表达的变化。结果　右美托咪定对于缺氧无糖（OGD）损伤处理的神经元具有明显保护效果。右美托咪定预处理显著降低OGD损伤神经元中的磷酸化p38MAPK蛋白表达, p38MAPK抑制剂SB203580能模拟DEX的神经保护作用，使细胞存活率升高。结论　右美托咪定预处理对于大鼠原代皮层神经元OGD损伤具有明显的保护效果。其机制可能与通过降低磷酸化p38MAPK表达有关。

Abstract

Objective　To study the protection and mechanism of dexmedetomidine preconditioning against neuronal injury related to oxygen–glucose deprivation(OGD).　Methods　Cortical neurons from the embryonic day 16~18 rats were cultured. With mimicking a cerebral ischemia in vitro, OGD was performed in the pretreated cells. Neuron injury was assessed by MTT. Protein expression of p-p38 was examined by Western blot.　Results　Dexmedetomidine preconditioning protected the dose-dependent cortical neurons from OGD injury.　Conclusions　Dexmedetomidine preconditioning protects the cortical neuron from OGD injury; inhibition of p38MAPK pathway maybe one of the mechanisms responsible for this effect.

导出引用

李红英, 张建杏, 王研, 于卫, 周国斌. 右美托咪定对大鼠神经元缺氧无糖损伤保护作用的实验研究[J]. 中国临床解剖学杂志. 2014, 32(4): 455-457 https://doi.org/10.13418/j.issn.1001-165x.2014.04.020

LI Gong-Yang, ZHANG Jian-Xing, WANG Xing, XU Wei, ZHOU Guo-Bin. Protection and mechanism of dexmedetomidine preconditioning against neuronal injury related to oxygen-glucose deprivation[J]. Chinese Journal of Clinical Anatomy. 2014, 32(4): 455-457 https://doi.org/10.13418/j.issn.1001-165x.2014.04.020

中图分类号： R971

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