论文部分内容阅读
目的研究自由基清除剂依达拉奉对大鼠癫痫持续状态(SE)后神经元细胞凋亡的影响。方法采用氯化锂-匹罗卡品大鼠癫痫持续状态模型,实验Wistar大鼠随机分为实验组(72只)和对照组(C组,6只),实验组分为模型组(M组)、依达拉奉单药治疗组(ED组)、联合地西泮治疗组(ED+DI),每组按照时间点分为4个亚组(12 h、24 h7、2 h、7 d)。免疫组化法检测大鼠脑组织的Bcl-2蛋白表达,及TUNEL法检测细胞凋亡的情况。结果 Bcl-2蛋白表达与对照组相比,M组12 h达高峰,24 h开始减少,7 d减至基础水平(P<0.05)。而依达拉奉单药和联合地西泮治疗组与之比较,变化趋势相同但Bcl-2表达增多(P<0.05);M组TUNEL染色阳性细胞极多,12 h开始上升,48 h达高峰,之后有下降趋势(P<0.01)。ED组TUNEL染色阳性细胞数值变化趋势相同但低于M组(P<0.01),高于ED+DI组;ED+DI组与C相比仍有统计学意义(P<0.05)。结论依达拉奉对氯化锂-匹罗卡品大鼠癫痫持续状态所致脑损伤具有保护作用,其机制可能通过清除自由基上调Bcl-2蛋白表达及减少神经元细胞凋亡,联合地西泮治疗效果更显著。
Objective To study the effect of free radical scavenger edaravone on neuronal apoptosis after epileptic seizure (SE) in rats. Methods The model of status epilepticus in rats treated with lithium chloride-pilocarpine was established. The experimental Wistar rats were randomly divided into experimental group (72 rats) and control group (C rats, 6 rats). The experimental rats were divided into model group (M group ), Edaravone monotherapy group (ED group) and diazepam treatment group (ED + DI). Each group was divided into 4 subgroups according to the time point (12 h, 24 h 7, 2 h, 7 d ). Immunohistochemistry was used to detect the expression of Bcl-2 protein in rat brain and the apoptosis was detected by TUNEL. Results Compared with the control group, the expression of Bcl-2 protein peaked at 12 h in M group, decreased at 24 h, and decreased to basal level at 7 d (P <0.05). Compared with Edaravone monotherapy and diazepam treatment group, the change trend was the same but the expression of Bcl-2 was increased (P <0.05); TUNEL staining positive cells in M group were very much and began to rise at 12 h, Peak, then a downward trend (P <0.01). The trend of TUNEL positive cells in ED group was the same but lower than that of M group (P <0.01), higher than that of ED + DI group. There was still significant difference between ED + DI group and C group (P <0.05). Conclusion Edaravone has a protective effect on brain damage induced by status epilepticus in lithium chloride-pilocarpine rats. The mechanism may be through up-regulating the expression of Bcl-2 protein and reducing the apoptosis of neurons in free radicals, The effect of diazepam is more pronounced.