Edaravone protects primary-cultured rat cortical neurons from ketamine-induced apoptosis via reducing oxidative stress and activating PI3K/Akt signal pathway

Publication date: Available online 7 September 2019Source: Molecular and Cellular NeuroscienceAuthor(s): Qianqian Li, Zhengguo Qiu, Yang Lu, Pan Lu, Jieqiong Wen, Kui Wang, Xijuan Zhao, Rong Li, Hong Zhang, Yan Zhang, Pengyu Jia, Pei Fan, Yuanyuan Zhang, Shuyue Zhang, Haixia Lv, Xinlin Chen, Yong Liu, Pengbo ZhangAbstractKetamine caused neuroapoptosis in the development of rat brain, in which oxidative stress play an important role. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger, exerts neuroprotective effects in many neurological disease models. Here we investigated whether edaravone protects primary-cultured neurons against ketamine-induced apoptosis and its potential mechanism. Edaravone increased neuronal viability, decreased neuronal apoptosis, increased the ratio of Bcl-2/Bax after ketamine exposure. Edaravone also increased superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) level in ketamine-exposed neurons. In addition, edaravone increased protein levels of phosphorylated-protein kinase B (p-Akt), phosphorylated-glycogen synthase kinase-3β (p-GSK-3β) and phosphorylated-forkhead box protein O1 (p-FoxO1) in ketamine-exposed neurons. The neuroprotective effects of edaravone were reversed by LY294002, a specific phosphatidylinositol 3-kinase (PI3K) inhibitor. These findings demonstrated that edaravone protected neurons against ketamine-induced apoptosis by diminishing oxidative stress and activating PI3K/Akt signal pathway...
Source: Molecular and Cellular Neuroscience - Category: Neuroscience Source Type: research