依达拉奉对血管性痴呆大鼠海马氧化损伤和迟发性神经元死亡的影响  

Effect of edaravone on oxidative stress and neuronal death after vascular dementia

作　　者：王玲[1] 孙晓菊[1] 黄衍军[2] 

机构地区：[1]华中科技大学同济医学院附属梨园医院,湖北武昌430077 [2]武汉大学医学部,湖北武汉430070

出　　处：《中国医院药学杂志》2009年第19期1639-1642,共4页Chinese Journal of Hospital Pharmacy

摘　　要：目的:研究脑缺血大鼠海马氧化损伤状况及依达拉奉对血管性痴呆(VD)的治疗意义。方法:双侧颈总动脉结扎制备VD模型,成模15d后,皮下注射依达拉奉治疗45d;通过生物化学法检测海马SOD、MDA含量,HE染色观察海马形态,TUNEL法检测海马神经元凋亡,逆转录PCR检测海马bax mRNA,Y-型迷宫测试大鼠认知能力。结果:VD模型组大鼠长期存在海马的MDA增多和SOD减少,bax mRNA上调,CA1区凋亡细胞率增高和认知能力的下降;与VD模型组相比,依达拉奉组海马MDA降低,SOD上调,bax mRNA下调,大鼠的认知能力改善。结论:氧化损伤在脑缺血后的持续存在,可能是VD形成的重要因素;依达拉奉通过清除自由基、抑制氧化损伤,减少了海马神经元的迟发性死亡,从而改善VD大鼠的认知能力。OBJECTIVE To investigate the oxidative damage following brain ischemia, and the effect of edaravone on rats suffering vascular dementia （XD）. METHODS A chronic ischemia model was made through permanent bilateral carotid arter ies occlusion. Fifteen days later, rats in edaravone-treated group were iniected with 3 mg·kg^-1 edaravone subcutaneously once a day in another 45 days. Then, the hippocampuses were prepared for measure of SOD and MDA （biochemical methods） ,morphological observation （HE staining）, test of bax mRNA （reverse-transcriptase PCR） and cognitive assessment （Ytype maze）. RESULTS In the hippocampus,MDA was increased,SOD was decreased, bax mRNA was upregulated, percentage of TUNEL （ ＋ ） cells in CA1 was increased,and cognitive damage was enhanced by the ischemia. But edaravone treatment partly retrieved all of those damages significantly （P〈0. 01）. CONCLUSION Oxidative stress exists persistently after ischemia, which maybe an important cause to the dementia; edaravone can improve cognitive functions of VD rats, partly through suppressing oxidative damage and delayed neuronal death in hippocampus.

关 键 词：血管性痴呆 依达拉奉 氧化应激 

分 类 号：R969[医药卫生—药理学]