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

作者：He, Yue; Zhou, Ailing^*; Jiang, Wei

来源：Neural Regeneration Research, 2013, 8(29): 2744-2753.

DOI：10.3969/j.issn.1673-5374.2013.29.006

• neural regeneration
• brain injury
• hippocampus
• neurons
• Toll like receptor 4
• phosphatidylinositol 3 kinase/protein kinase B-glycogen synthase kinase 3 beta
• apoptosis
• grants-supported paper
• neuroregeneration

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 synthase kinase 3 beta (GSK-3 beta) 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-AKT(Ser473) and P-GSK-3 beta(Ser9) in hippocampal neurons stimulated by lipopolysaccharide 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-3 beta inhibitor, LiCl, decreased before intervention with lipopolysaccharide, but increased after treatment with the AKT inhibitor, LY294002. These findings suggest that the TLR4-PI3K/AKT-GSK3 beta signaling pathway may be involved in lipopolysaccharide-induced apoptosis of hippocampal neurons.

• 出版日期2013-10
• 单位南通大学