Protective Effect of Edaravone on Glutamate-Induced Neurotoxicity in Spiral Ganglion Neurons
作者
Bai, XH;Zhang, C;Chen, AP;Liu, WW;Li, JF;Sun, Q;Wang, HB
作者单位
[Bai, Xiaohui; Zhang, Chi; Chen, Aiping; Liu, Wenwen; Li, Jianfeng; Wang, Haibo] Shandong Univ, Shandong Prov Hosp, Dept Otolaryngol Head & Neck Surg, Jinan 250021, Peoples R China.;-;[Bai, Xiaohui; Zhang, Chi; Chen, Aiping; Liu, Wenwen; Li, Jianfeng; Wang, Haibo] Shandong Prov Key Lab Otol, Jinan 250022, Peoples R China.;-;[Sun, Qian] Emory Univ, Human Genet Dept, Atlanta, GA 30322 USA.
摘要
"excitotoxicity" and lead to neuronal death. As bipolar neurons, spiral ganglion neurons (SGNs) function as a "bridge" in transmitting auditory information from the ear to the brain and can be damaged by excessive glutamate which results in sensorineural hearing loss. In this study, edaravone, a free radical scavenger, elicited both preventative and therapeutic effects on SGNs against glutamate-induced cell damage that was tested by MTT assay and trypan blue staining. Ho. 33342 and PI double staining revealed that apoptosis as well as necrosis took place during glutamate treatment, and apoptosis was the main type of cell death. Oxidative stress played an important role in glutamate-induced cell damage but pretreatment with edaravone alleviated cell death. Results of western blot demonstrated that mechanisms underlying the toxicity of glutamate and the protection of edaravone were related to the PI3K pathway and Bcl-2 protein family.
关键词
FREE-RADICAL SCAVENGER; DEVELOPING RAT COCHLEA; GUINEA-PIG; REPERFUSION INJURY; INDUCED OTOTOXICITY; IN-VIVO; ISCHEMIA; INFARCTION; APOPTOSIS; TRAUMA
基本信息
