Edaravone alleviates hypoxia-induced injury by inhibiting PI3K/AKT signaling pathway in HTR-8/SVneo cells

Abstract

Abstract Objective This study aims to discuss the possible therapeutic effect of EDA against hypoxia-induced injury in preeclampsia. Materials and methods Placenta tissues were isolated from pregnant women with or without preeclampsia (PE), and the levels of hypoxia inducible factor (HIF-1α), P-AKT, AKT and PI3K proteins were analyzed by western blotting. The human trophoblast cell line HTR-8/SVneo was treated with cobalt chloride (CoCl2) to establish an in vitro anoxia model. The proliferation, apoptosis and reactive oxygen species (ROS) production rates in the anoxic cells with/out EDA treatment were measured by standard techniques. Results HIF-1α, P-AKT, AKT and PI3K protein levels were significantly higher in the placenta of the PE revlative to the control group. EDA alleviated the CoCl2-induced decrease in the viability of HTR-8/SVneo cells, along with apoptosis and ROS production. EDA also reversed the activation of PI3K/AKT pathway in the CoCl2-treated trophoblasts. Conclusion EDA protected trophoblasts against hypoxic injury by blocking the PI3K/AKT pathway and is a promising therapeutic option for PE.