PI3K/Akt信号转导通路在绞股蓝皂苷拮抗谷氨酸诱导胎鼠大脑皮层神经元氧化性损伤中的作用

山东大学学报(医学版) ›› 2011, Vol. 49 ›› Issue (10): 107-112.

PI3K/Akt信号转导通路在绞股蓝皂苷拮抗谷氨酸诱导胎鼠大脑皮层神经元氧化性损伤中的作用

张道来1，孙涛2，谢珊珊2，王玉卓2，冯玉新2，辛华2

1.滨州医学院药学院干细胞与组织工程研究所，山东烟台 264003；
2.山东大学医学院细胞生物学研究所，济南 250012

收稿日期:2011-05-13 出版日期:2011-10-10 发布日期:2011-10-10
通讯作者: 辛华(1950- )，女，教授，主要从事神经损伤与保护机制的研究。E-mail:xinhua@sdu.edu.cn
作者简介:张道来(1984- )，男，助教，主要从事细胞生物学的研究。
基金资助:
山东省自然科学基金资助项目(Y2006C41)

Role of the PI3K/Akt signal pathway in gypenosides antagonizing glutamate-induced oxidative damage to fetal rats’cerebral cortical neurons

ZHANG Dao-lai1, SUN Tao2, XIE Shan-shan2, WANG Yu-zhuo2, FENG Yu-xin2, XIN Hua2

1. Institute of Stem Cells and Tissue Engineering, College of Pharmacy, Binzhou Medical University,
Yantai 264003, Shandong, China;
2. Institute of Cell Biology, School of Medicine, Shandong University, Jinan 250012, China

Received:2011-05-13 Online:2011-10-10 Published:2011-10-10

摘要/Abstract

摘要：

目的应用磷脂酰肌醇3位羟基激酶(PI3K)的特异性阻断剂LY294002，研究PI3K/Akt信号转导通路在绞股蓝皂苷(GPs)拮抗谷氨酸(Glu)诱导胎鼠大脑皮层神经元氧化性损伤中的作用。方法以体外原代培养的14～15d胎鼠大脑皮层神经元为研究对象，用相差显微镜进行形态学观察，MTT法检测神经元存活率，流式细胞仪检测神经元凋亡率，Western blot法检测磷酸化Akt和总Akt的表达，分析PI3K/Akt信号转导通路在GPs拮抗Glu诱导神经元氧化性损伤中的作用。结果 GPs可抑制Glu诱导的胎鼠大脑皮层神经元氧化性损伤，使神经元存活率上升，凋亡率降低，磷酸化Akt表达增加，PI3K的特异性抑制剂LY294002明显抑制了GPs对神经元的保护作用。结论绞股蓝皂苷激活了PI3K/Akt信号转导通路，拮抗谷氨酸诱导的胎鼠大脑皮层神经元氧化性损伤。

关键词: 绞股蓝皂苷；谷氨酸；大脑皮层; 神经元；1-磷脂酰肌醇3-激酶；LY294002

Abstract:

Objective To investigate the role of the phosphatidylinositol 3-OH kinase(PI3K)/Akt signal pathway in gypenosides(GPs) antagonizing glutamate(Glu)-induced oxidative damage to fetal rats′ cerebral cortical neurons, using LY294002, a specific inhibitor of PI3K. Methods Primary culture of 14-15d fetal rats′ cerebral cortical neurons in vitro was used in this study. Morphology was observed by a phase contrast microscope, neuronal survival was detected by MTT assay, and the neuronal apoptotic rate was detected by flow cytometry. Expressions of phosphorylated Akt and total Akt were detected by Western blot. Results GPs inhibited Glu-induced oxidative damage to fetal rats′ cerebral cortical neurons, increased the survival rate of neurons and expression of phospho-Akt, and decreased neuronal apoptosis. LY294002, the specific inhibitor of PI3K, significantly inhibited such protective effect of GPs. Conclusion GPs activate the PI3K/Akt signal pathway to antagonize Glu-induced oxidative neurotoxicity.

Key words: Gypenosides; Glutamic acid; Cerebral cortex; Neurons; 1-Phosphatidylinositol 3-OH kinase; LY294002

中图分类号:

R285.5

张道来1，孙涛2，谢珊珊2，王玉卓2，冯玉新2，辛华2. PI3K/Akt信号转导通路在绞股蓝皂苷拮抗谷氨酸诱导胎鼠大脑皮层神经元氧化性损伤中的作用[J]. 山东大学学报(医学版), 2011, 49(10): 107-112.

ZHANG Dao-lai1, SUN Tao2, XIE Shan-shan2, WANG Yu-zhuo2, FENG Yu-xin2, XIN Hua2. Role of the PI3K/Akt signal pathway in gypenosides antagonizing glutamate-induced oxidative damage to fetal rats’cerebral cortical neurons[J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2011, 49(10): 107-112.

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