Protective effect of EGb761 against Aβ1-42 -induced SHSY5Y cells injury and blood-brain barrier disruption via regulating Akt/Nrf2 signaling pathway

Purpose: Alzheimer’s disease (AD) is a common in the world caused by deposition brain parenchyma, accumulation of beta amyloid which leads to blood barrier (BBB) disruption. Regardless enough progress treatment AD, principal mechanism BBB injury yet not clear.Methods: In this study we examined impact EGb761on Aβ 1-42-induced SH-SY5Y cells vitro model AD. Cell viability was assessed using MTT assay, flow cytometry used check rate cell apoptosis, ROS generation and leakage measuring level fluorescence Aβ-induced reactive oxygen species kit assay permeability mRNA levels Bax, Bcl-2, caspase-3 measured RT-qPCR. Furthermore, western blot analysis measure protein expressions Akt, Nrf2 HO-1 cells.Results: The effect EGb761 investigated on apoptosis induced 1-42 andgeneration found that plays protective role against 1-42. decreased significantly with EGb761. reduced considerably when treated expression Caspase-3 Bax while Bcl-2 were markedly increased cells. Also, an p-Akt, (nucleus) observed cells.Conclusion: It can be concluded from these results could play byinhibiting protect AD via activating Akt/Nrf2signaling pathway. Our suggested might therapeutic agent for preventionand