关键词: 脑创伤, Edaravone, ERK1/2, 细胞凋亡

Abstract: Objective To study the effect and potential mechanism of Edaravone on extracellular signal-regulated kinase 1/2 (ERK1/2) signal pathway and neuron apoptosis after traumatic brain injury(TBI). Methods Male Sprague-Dawley rats(n=120) were divided randomly into three groups:sham operation group (A group, n=24 ), traumatic group (B group, n=48), Edaravone treatment group (C group, n=48). TBI rat model was established accor ding to the description of Marmarou's diffused brain injury. At different time points (1, 6, 24, 48,72 h) after operation, the malondialdehyde (MDA) contents in cortex were measured with spectrophotometry, the qualities and quantities of p-ERK1/2, Bax and bcl-2 were detected by immunohistochemistry and Western-Blot, the quantities of neuron apoptosis were observed with TUNEL method. Results Compared with sham group，MDA contents(6～72 h post trauma)，the expression levels of p-ERK1/2（1～48 h post trauma)，the rates of Bax /bcl-2（6～48 h post trauma) and the apoptotic cells(6～72 h post trauma)in the cortex were significantly enhanced (p<0.05) following TBI；Compared with traumatic group，the above mentioned indexes in Edaravone treatment group were decreased obviously (p<0.05).Conclusions Edaravone can dramatically alleviate neuron apoptosis. The one of mechanisms is related to its scavenging oxygen free radical and down-regulation effect on ERK1/2 signal pathway.

Key words: Traumatic brain injury, Edaravone, ERK1/2, Apoptosis