论文部分内容阅读
目的观察依达拉奉对大鼠癫痫持续状态后脑内自由基及海马神经元凋亡的影响及可能机制。方法采用氯化锂-匹罗卡品大鼠癫痫持续状态模型,成年雄性Wistar大鼠54只随机分为实验组48只和对照组6只,实验组分为模型组、依达拉奉治疗组,每组按照时间点分为4个亚组(12、24、72 h,7 d)。化学比色法测定脑组织匀浆中超氧化物歧化酶(SOD)活性、丙二醛(MDA)的含量,免疫组织化学法检测大鼠脑组织c-fos蛋白表达。结果与对照组相比,模型组的SOD活性在12 h开始下降,72 h时最低(P<0.01),7 d时恢复正常;依达拉奉治疗组与之趋势相同,但各时间点均高于模型组。模型组的MDA含量和大鼠脑组织的c-fos蛋白表达在各时间点均高于对照组(P<0.05);依达拉奉治疗组与之趋势相同,但在24、72 h低于模型组(P<0.05)。结论依达拉奉可以清除自由基,减少海马神经元的凋亡,对癫痫持续状态后的脑损伤有一定的保护作用。
Objective To observe the effect of edaravone on apoptosis of free radicals and hippocampal neurons in rat brain after status epilepticus and its possible mechanism. Methods Fifty-four male Wistar rats were randomly divided into experimental group (n = 48) and control group (n = 6). The experimental group was divided into model group, edaravone group , Each group was divided into 4 sub-groups according to the time point (12, 24, 72 h, 7 d). The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in brain homogenate were measured by chemical colorimetry. The expression of c-fos protein in rat brain was detected by immunohistochemistry. Results Compared with the control group, the SOD activity of the model group began to decrease at 12 h and reached the lowest at 72 h (P <0.01), and returned to normal at 7 d. The trend of edaravone group was the same, but at each time point Higher than the model group. The content of MDA in model group and the expression of c-fos protein in rat brain tissue were higher than those in control group at each time point (P <0.05). Edaravone treatment group had the same trend but decreased at 24 and 72 h Model group (P <0.05). Conclusion Edaravone can scavenge free radicals, reduce the apoptosis of hippocampal neurons, and have a protective effect on brain damage after status epilepticus.