Effects of Edaravone on Expression of p-ERK1/2 in Cerebral Ischemia/Reperfusion Injury

Objective:To investigate whether edaravone can reduce cerebral ischemia/reperfusion injury,and the role of p-ERK1/2 in this precess thereof. Methods:One hundred and eighty ICR male mice were divided into sham-operated group,saline treatment group and edaravone treatment group. Mice in the three groups were designated as subgroups,30 min,3 h,6 h,24 h and 48 h after cerebral ischemia/reperfusion. The mouse models of focal cerebral ischemia/reperfusion were established by middle cerebral atery occlusion. In the treatment group edaravone (3 mg/kg) was injected through vena caudalis immediately after ischemia/reperfusion. Then it was medicated once every 12 h. The neurological score was estimated at 24 h. Western blot and immunochemistry were used to evaluate the expression level and regional distribution of p-ERK1/2. Apoptosis neurons were detected by TUNEL method. Results:Compared with sham-operated group and saline treatment group,mouse neural behavioral scores were decreased significantly in edaravone treatment group (P 0.05); the immunoreactive cells and protein expression of p-ERK1/2 were decreased significantly (P 0.05); apoptotic cells also were decreased (P 0.05). Conclusion:Edaravone can inhibit the ERK1/2 signaling pathway,which is closely related to oxidative stress,and significantly reduce cerebral ischemia-reperfusion injury.