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CLC number: R614.1

On-line Access: 2017-09-05

Received: 2016-10-19

Revision Accepted: 2016-12-18

Crosschecked: 2017-08-16

Cited: 0

Clicked: 1865

Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Ke-zhong Li

http://orcid.org/0000-0003-0081-6459

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Journal of Zhejiang University SCIENCE B 2017 Vol.18 No.9 P.789-796

http://doi.org/10.1631/jzus.B1600476


Neuroprotection of dexmedetomidine against propofol-induced neuroapoptosis partly mediated by PI3K/Akt pathway in hippocampal neurons of fetal rat


Author(s):  Ning Zhang, Quan-ping Su, Wei-xia Zhang, Nian-jun Shi, Hao Zhang, Ling-ping Wang, Zhong-kai Liu, Ke-zhong Li

Affiliation(s):  Department of Anesthesiology, the Second Hospital of Shandong University, Jinan 250033, China; more

Corresponding email(s):   likezhongsdu@163.com

Key Words:  Dexmedetomidine, Propofol, Neuroapoptosis, PI3K/Akt


Ning Zhang, Quan-ping Su, Wei-xia Zhang, Nian-jun Shi, Hao Zhang, Ling-ping Wang, Zhong-kai Liu, Ke-zhong Li. Neuroprotection of dexmedetomidine against propofol-induced neuroapoptosis partly mediated by PI3K/Akt pathway in hippocampal neurons of fetal rat[J]. Journal of Zhejiang University Science B, 2017, 18(9): 789-796.

@article{title="Neuroprotection of dexmedetomidine against propofol-induced neuroapoptosis partly mediated by PI3K/Akt pathway in hippocampal neurons of fetal rat",
author="Ning Zhang, Quan-ping Su, Wei-xia Zhang, Nian-jun Shi, Hao Zhang, Ling-ping Wang, Zhong-kai Liu, Ke-zhong Li",
journal="Journal of Zhejiang University Science B",
volume="18",
number="9",
pages="789-796",
year="2017",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1600476"
}

%0 Journal Article
%T Neuroprotection of dexmedetomidine against propofol-induced neuroapoptosis partly mediated by PI3K/Akt pathway in hippocampal neurons of fetal rat
%A Ning Zhang
%A Quan-ping Su
%A Wei-xia Zhang
%A Nian-jun Shi
%A Hao Zhang
%A Ling-ping Wang
%A Zhong-kai Liu
%A Ke-zhong Li
%J Journal of Zhejiang University SCIENCE B
%V 18
%N 9
%P 789-796
%@ 1673-1581
%D 2017
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1600476

TY - JOUR
T1 - Neuroprotection of dexmedetomidine against propofol-induced neuroapoptosis partly mediated by PI3K/Akt pathway in hippocampal neurons of fetal rat
A1 - Ning Zhang
A1 - Quan-ping Su
A1 - Wei-xia Zhang
A1 - Nian-jun Shi
A1 - Hao Zhang
A1 - Ling-ping Wang
A1 - Zhong-kai Liu
A1 - Ke-zhong Li
J0 - Journal of Zhejiang University Science B
VL - 18
IS - 9
SP - 789
EP - 796
%@ 1673-1581
Y1 - 2017
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1600476


Abstract: 
The aim was to investigate how the PI3K/Akt pathway is involved in the protection of dexmedetomidine against propofol. The hippocampal neurons from fetal rats were separated and cultured in a neurobasal medium. Cell viability was assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Then neurons were pretreated with different concentrations of dexmedetomidine before 100 μmol/L propofol was added. Akt, phospho-Akt (p-Akt), Bad, phospho-Bad (p-Bad), and Bcl-xL were detected by Western blot. Also, neurons were pretreated with dexmedetomidine alone or given the inhibitor LY294002 before dexmedetomidine pretreatment, and then propofol was added for 3 h. The results demonstrated that propofol decreased the cell viability and the expression of p-Akt and p-Bad proteins, increased the level of Bad, and reduced the ratio of Bcl-xL/Bad. dexmedetomidine pretreatment could reverse these effects. The enhancement of p-Akt and p-Bad induced by dexmedetomidine was prevented by LY294002. These results showed that dexmedetomidine potently protected the developing neuron and this protection may be partly mediated by the PI3K/Akt pathway.

PI3K/Akt信号通路部分参与了右美托咪定对异丙酚诱导的胎鼠海马神经元凋亡的保护作用

目的:研究PI3K/Akt信号通路是否参与了右美托咪定对异丙酚诱导的胎鼠海马神经元凋亡的保护作用,并初步探讨可能的作用机制。
创新点:首次利用胎鼠海马神经元研究发现右美托咪定对异丙酚诱导的神经元凋亡作用部分是由PI3K/Akt信号通路介导的。
方法:首先分离胎鼠海马神经元并鉴定。使用MTT法检测异丙酚对神经元活性的影响。然后将神经元分为不同的组,分别用0.1、1、10和100 µmol/L右美托咪定预处理细胞,然后加入100 µmol/L的异丙酚继续培养,同时设异丙酚组和正常对照组。使用蛋白质印迹(Western blot)方法检测Akt、p-Akt、Bad、p-Bad和Bcl-xL的表达变化。在100 µmol/L右美托咪定预处理前加入LY294002,进一步研究PI3K/Akt途径是否参与了右美托咪定对异丙酚诱导的胎鼠海马神经元凋亡的保护作用。
结论:实验结果显示,异丙酚明显降低了神经元的细胞活性及p-Akt和p-Bad的表达水平,增加了Bad的表达,从而Bcl-xL/Bad的比率升高。100 µmol/L右美托咪定预处理可以逆转这种效果。LY294002可以抑制右美托咪定的保护作用,说明右美托咪定对异丙酚诱导的胎鼠海马神经元凋亡的保护作用部分是由PI3K/Akt信号通路介导的。

关键词:右美托咪定;异丙酚;神经凋亡;PI3K/Akt

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

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