依达拉奉对癫痫持续状态大鼠神经元凋亡及XIAP、Caspase-3表达的影响

Effects of Edaravone on Neuronal Apoptosis and Expression of XIAP and Caspase-3 in Rats with Status Epilepticus

目的探讨自由基清除剂依达拉奉对于大鼠癫痫持续状态后所导致的神经元凋亡和XIAP、Caspase-3的影响。方法对2015年9月—2017年9月雄性Wistar大鼠共54只展开研究,将该组所有大鼠随机分为对照组(N组)、模型组(M组)和依达拉奉组(ED组)3组,其中对照组6只,后两组再分为6、12、24、48 h 4个亚组,每个亚组6只。采用氯化锂-匹罗卡品制备SE动物模型,大鼠海马神经元凋亡检测采用TUNEL法来完成,同时对XIAP、Caspase-3蛋白表达采用免疫组化来进行检测。结果在6 h内SE后M组主要有阳性TUNEL、XIAP和Caspase-3细胞,TUNEL和Caspase-3表达高峰是在24 h左右(43.17±1.424),(35.26±1.428);XIAP表达高峰在12 h(40.68±2.817),两组差异有统计学意义(P=0.013)。ED组与M组相比,在12、24 h和48 h,TUNEL和Caspase-3阳性细胞数减少(P<0.05),XIAP阳性细胞数有所增加(P<0.05)。结论依达拉奉在大鼠神经元凋亡下持续癫痫状态中应用,可以提高XIAP蛋白的表达,抑制Caspase-3蛋白的表达,从而对神经元损伤提供保护。

Objective To investigate the effects of free radical scavenger edaravone on neuronal apoptosis and XIAP and Caspase-3 induced by epilepticus in rats. Methods A total of 54 male Wistar rats from September 2015 to September 2017 were enrolled. All rats in this group were randomly divided into control group (N group), model group (M group) and edaravone group (ED group), there were three groups, including 6 in the control group. The latter two groups were subdivided into four subgroups of 6 h, 12 h, 24 h and 48 h, with 6 in each subgroup. The animal model of SE was prepared by using lithium chloride-pilocarpine. The apoptosis of rat hippocampal neurons was detected by TUNEL method. The expression of XIAP and Caspase-3 protein was detected by immunohistochemistry. Results After 6 hours, the main group had positive TUNEL, XIAP and Caspase-3 cells peak expression of TUNEL and Caspase-3 was about 24 h (43.17±1.424),(35.26±1.428);the peak of XIAP expression was 12 h (40.68±2.817), the different was statistically significant(P=0.013). Compared with the M group, the number of TUNEL and Caspase-3 positive cells decreased in the ED group at 12 h, 24 h and 48 h (P<0.05), and the number of XIAP positive cells increased (P<0.05). Conclusion The application of edaravone in the continuous epilepsy state of rat neuronal apoptosis can increase the expression of XIAP protein and inhibit the expression of Caspase-3 protein, thus providing protection for neuronal damage.