依达拉奉预处理对大鼠脑干缺血再灌注损伤后MDA、SOD的影响

Effect of Edaravone pretreatment on MDA and SOD of brainstem after ischemical reperfusion injury in rats

目的:用依达拉奉(EDA)对大鼠预处理,观察其对大鼠脑干缺血再灌注损伤后丙二醛(MDA)、超氧化物歧化酶(SOD)表达水平的影响,探讨研究EDA对脑干缺血再灌注损伤的保护作用,为临床应用提供实验依据。方法 :将25只SD大鼠随机分为3组,即对照组5只、缺血再灌注组和依达拉奉预处理组各10只。根据缺血时间的不同,把缺血再灌注组和依达拉奉预处理组分为缺血1 h再灌注7 h和缺血3 h再灌注5 h两个亚组,每亚组5只大鼠。其中对照组:暴露基底动脉(BA)第一无分支区和第二无分支区,观察8 h;缺血再灌注组:用微型动脉夹夹闭基底动脉第一无分支区和第二无分支区,分别使之缺血1 h和3 h,再分别灌注7 h和5 h;依达拉奉预处理组:各亚组实验前10 min于大鼠尾静脉注射依达拉奉6 mg/kg,其它同缺血再灌注组。HE染色观察各组脑干组织的病理改变。测定各组大鼠脑干中MDA及SOD表达水平。结果:在缺血1 h时,与假手术组和预处理组比较,缺血再灌注组MDA含量明显升高,SOD含量明显降低,差异均具有统计学意义(P<0.05)。在缺血3h时,与假手术组比较,预处理组和缺血再灌注组MDA含量明显升高,SOD含量明显降低,差异均有统计学意义(P<0.05);与预处理组比较,缺血再灌注组MDA含量明显升高,SOD含量明显降低,差异均有统计学意义(P<0.05)。结论:依达拉奉预处理通过减少MDA含量、增加SOD活性,清除自由基、对抗脂质过氧化等机制,对大鼠脑干缺血再灌注具有一定的保护作用。

Objective： To evaluate the protective effect of Edaravone on brainstem after ischemia/reperfusion injury and to provide experimental evidence for clinic, rats were pretreated with Edaravone and its effect on MDA and SOD were studied. Methods： 25 SD rats used in experimental animals were divided into 3 groups at random：sham operation group,brainstem ischemia reperfusion group and Edaravone pretreatment group（n = 10）. According to different ischemia time period, rats in ischemia/reperfusion group and Edaravone pretreatment group were further divided evenly into ischemia 1 h/reperfusion 7 h and ischemia 3 h/reperfusion 5 h subgroups, respectively.The 1st and the 2nd basilar artery without branch areas were exposed, and animals were observed without any treatment for 8 h in normal group, the arteries were clamped with Micro-bulldog clamp to create ischemia for 1 h/reperfusion 7 h（5 animals） and ischemia for and 3 h/reperfusion 7 h（5 animals） respectively in ischemia reperfusion group, and animals in Edaravone pretreatment group were given Edaravone（6 mg/kg） by tail vein injection 10 min before ischemia/reperfusion as described in ischemia/reperfusion group. The histology of brainstems after HE staining were compared, the brainstem tissues at various stages was observed by light microscope at 200 magnification. The activities of SOD and the contents of MDA at various subgroups were measured with spectrophotometry. Results： When the time on ischemia 1 h, compared with the normal group and pretreatment group, the contents of MDA were significantly increased and the contents of SOD were obviously decreased in ischemia reperfusion group, the differences all had statistical significance（P 〈 0.05）. When the time on ischemia 3 h, compared with the normal group, the contents of MDA were significantly increased and the contents of SOD were obviously decreased in pretreatment group and ischemia reperfusion group, the differences all had statistical significance（P 〈 0.05）; Compared with the pretreatment group, the contents of MDA were significantly increased and the contents of SOD were obviously decreased in ischemia reperfusion group, the differences all had statistical significance（P 〈 0.05）. Conclusion： Edaravone played a tremendous and definite role in ischemia reperfusion injury of brainstem in rats. Its mechanism has to do with the reduced levels of MDA, the increased activity of SOD, the removal of oxyradicals, and the inhibited overoxidation of lipid.