title: Toll-like receptor 4-mediated signaling participates in apoptosis of hippocampal neurons.
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-AKT(Ser473) and P-GSK-3β(Ser9) in hippocampal neurons stimulated by lipopo-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, creased before intervention with lipopolysaccharide, but increased after treatment with the AKT hibitor, LY294002. These findings suggest that the TLR4-PI3K/AKT-GSK3β signaling pathway may be involved in lipopolysaccharide-induced apoptosis of hippocampal neurons.
authors.affiliation: Department of Pathophysiology, Medical College, Nantong University, Nantong 226001, Jiangsu Province, China ; Department of Neurology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: He
authors.affiliation: Department of Pathophysiology, Medical College, Nantong University, Nantong 226001, Jiangsu Province, China.
authors.forename: Ailing
authors.initials: A
authors.lastname: Zhou
authors.affiliation: Department of Scientific Technology and Property, Nantong University, Nantong 226019, Jiangsu Province, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Jiang
keywords: Toll like receptor 4; apoptosis; brain injury; grants-supported paper; hippocampus; neural regeneration; neuro-regeneration; neurons; phosphatidylinositol 3 kinase/protein kinase B-glycogen synthase kinase 3β