论文部分内容阅读
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 the changes of free radical levels and the expression of brain-derived nerve growth factor (BDNF) in brain of acute cerebral ischemia rats and to explore its possible mechanism. Methods: Rat middle cerebral artery occlusion (MCAO) model was established by thread occlusion. The rats were divided into sham-operation group, normal saline control group and edaravone group. Each group is divided into 6,12,24,48 h4 subgroups. The contents of malondialdehyde (MDA) and superoxide dismutase (SOD) at different time points in each group were detected. The expression of BDNF mRNA and protein in cortex were detected by RT-PCR and Western-blot. Results: Edaravone intervention group significantly reduced MDA content (P <0.01), increased SOD activity (P <0.05), compared with the control group were statistically significant. BDNF mRNA expression in edaravone group was significantly higher than that in control group, and its expression was prolonged. BDNF protein expression was significantly increased compared with the control group. Conclusion: Edaravone can significantly reduce the content of MDA, increase the level of SOD, and have a clear role in scavenging free radicals. It can also significantly increase the expression of BDNF in cerebral cortex after ischemia-reperfusion. It is speculated that edaravone can also scavenge brain other than free radicals Protective effects.