摘要
目的:研究依达拉奉对脑缺血再灌注细胞损伤的影响及p-ERK1/2在此过程的作用。方法:将180只雄性ICR小鼠随机分为假手术组、生理盐水治疗组和依达拉奉治疗组。各组于缺血再灌注后分为30min、3h、6h、24h、48h等5个亚组。采用线栓法建立小鼠局灶性脑缺血再灌注模型。治疗组于脑缺血开始及再灌注后12h分别腹腔注射依达拉奉3mg/kg或等量生理盐水,于24h后进行小鼠神经功能学评分;应用免疫组织化学及Westernblot检测p-ERK1/2蛋白表达水平的变化;利用原位缺口末端标记法(TUNEL法)研究神经细胞凋亡的变化。结果:与生理盐水治疗组相比,依达拉奉治疗组小鼠神经行为学评分明显减少(P<0.05);p-ERK1/2免疫阳性细胞及蛋白表达明显减少(P<0.05);凋亡细胞也减少(P<0.05)。结论:依达拉奉能通过抑制与氧化应激有密切关系的p-ERK1/2信号通路显著减轻脑缺血再灌注损伤后神经细胞损伤。
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.
出处
《天津医药》
CAS
北大核心
2010年第4期310-312,355,共4页
Tianjin Medical Journal
基金
河北省自然科学基金资助项目(项目编号:C2009001247)
河北省教育厅重点课题(项目编号:ZH200803)
卫生部人类疾病比较医学重点实验室开放课题(项目编号:ZDS200801)
