JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2011, Vol. 49 ›› Issue (10): 107-112.

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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. 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

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

CLC Number: 

  • R285.5
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