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  

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

作　　者：张道来[1] 孙涛[2] 谢珊珊[2] 王玉卓[2] 冯玉新[2] 辛华[2] 

机构地区：[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

出　　处：《山东大学学报（医学版）》2011年第10期107-112,共6页Journal of Shandong University:Health Sciences

基　　金：山东省自然科学基金资助项目(Y2006C41)

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。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 14-15 d 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.

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 

分 类 号：R285.5[医药卫生—中药学]