Propofol protects hippocampal neurons from apoptosis in ischemic brain injury by increasing GLT-1 expression and inhibiting the activation of NMDAR via the JNK/Akt signaling pathway

摘要: Ischemic brain injury (IBI) can cause nerve injury and is a leading of morbidity mortality worldwide. The neuroprotective effects propofol against IBI have been previously demonstrated. However, the on hippocampal neurons are not yet entirely clear. In present study, models were established in hypoxia-exposed neuronal cells. Cell viability assay apoptosis performed to examine IBI. A significant decrease cell increase observed group compared with control group, accompanied by glial glutamate transporter-1 (GLT‑1) expression as determined RT-qPCR western blot analysis. reversed treatment. siRNA-mediated knockdown GLT‑1 cells led an apoptosis, Jun N-terminal kinase (JNK) activation N-methyl-D‑aspartate (NMDA) receptor (NR1 NR2B) activation, well Akt activation. RNA interference-mediated gene silencing viability, JNK NMDAR slightly agonist, anisomycin, inhibitor, LY294002, both significantly blocked caused overexpression NMDA. Collectively, our findings suggest that treatment protects enhancing inhibiting via JNK/Akt signaling pathway.