Neural Regeneration Research ›› 2013, Vol. 8 ›› Issue (29): 2744-2753.doi: 10.3969/j.issn.1673-5374.2013.29.006

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Toll-like receptor 4-mediated signaling participates in apoptosis of hippocampal neurons

Yue He1, 2, Ailing Zhou1, Wei Jiang3   

  1. 1 Department of Pathophysiology, Medical College, Nantong University, Nantong 226001, Jiangsu Province, China
    2 Department of Neurology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
    3 Department of Scientific Technology and Property, Nantong University, Nantong 226019, Jiangsu Province, China
  • Received:2013-06-08 Revised:2013-07-22 Online:2013-10-15 Published:2013-10-15
  • Contact: Ailing Zhou, Master, Professor, Department of Pathophysiology, Medical College, Nantong University, Nantong 226001, Jiangsu Province, China, ALZ@ntu.edu.cn.
  • About author:Yue He, Master.

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Abstract:

The phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling pathway is considered important for cell survival and has been shown to mediate various anti-apoptotic biological effects. This study explored the role of the Toll-like receptor 4 (TLR4)-mediated PI3K/AKT-glycogen syn-thase kinase 3β (GSK-3β) signaling pathways in lipopolysaccharide-induced apoptosis in a primary culture of hippocampal neurons. Results demonstrated that the apoptotic ratio of hippocampal neurons stimulated by lipopolysaccharide was significantly higher compared with the control group. Both the expression of P-AKTSer473 and P-GSK-3βSer9 in hippocampal neurons stimulated by lipo-polysaccharide decreased compared with the control, while the level of active Caspase-3 and the ratio of Bax/Bcl-2 were significantly increased. The level of active Caspase-3 and the ratio of Bax/Bcl-2 in hippocampal neurons treated with TLR4 antibody or the GSK-3β inhibitor, LiCl, de-creased before intervention with lipopolysaccharide, but increased after treatment with the AKT in-hibitor, LY294002. These findings suggest that the TLR4-PI3K/AKT-GSK3β signaling pathway may be involved in lipopolysaccharide-induced apoptosis of hippocampal neurons.