摘要
目的:研究依达拉奉对急性脑缺血大鼠脑自由基水平变化和脑源性神经生长因子(BDNF)表达的影响,并探讨其可能机制。方法:采用线栓法制备大鼠大脑中动脉缺血-再灌注模型,分为假手术组、生理盐水对照组和依达拉奉组。每组分为6、12、24、48h4个亚组。检测各组脑组织不同时间点丙二醛(MDA)、过氧化物歧化酶(SOD)含量,用RT-PCR和Western-blot检测皮层BDNF mRNA和蛋白质表达变化。结果:依达拉奉干预组显著降低MDA含量(P<0.01),增加SOD活性(P<0.05),与对照组比较有统计学差异。依达拉奉组BDNF mRNA表达水平明显高于对照组,表达时相延长。BDNF蛋白表达亦较对照组明显增加。结论:依达拉奉能显著降低MDA含量,增加SOD水平,具有明显的清除自由基作用,并能显著增加缺血再灌注后脑皮层BDNF的表达,推测依达拉奉还具有清除自由基以外的脑保护作用。
Objective:To study the effect of edaravone on contents of SOD,MDA and the expression of BDNF (brain-derived neurotrophic factor) in cerebral cortex after MCAO/R (middle cerebral artery occlusion/reperfusion) injury and its possible mechanisms in rats. Methods:A total of 72 healthy male rats were randomly divided into sham-operation group(n = 24), control group(n = 24) and edaravone treated group (n = 24). Each group was further divided into 6 h, 12 h,24 h and 48 h subgroups. The levels of SOD and MDA on each subgroup were examined. RT-PCR and Western-blot were used to detect the expression of BDNF mRNA and protein, respectively. Results:The contents of MDA and SOD were statistically significantly different between edaravone treated group and control group(P 〈 0.05). The expression of BDNF mRNA was statistically significantly different between edaravone therapy group and control group, so was the expression of BDMF protein levels. Conclusion:Edaravone is a potent scavenger of free radicals. Edar-avone increased the expression of BDNF after cerebral ischemia-reperfusion injury, which would play a new role in its neuroprotection.
出处
《南京医科大学学报(自然科学版)》
CAS
CSCD
北大核心
2009年第1期36-39,共4页
Journal of Nanjing Medical University(Natural Sciences)
基金
江苏省科技厅社会发展基金(BS2006007)