摘要
目的探讨Bcl-2、Caspase-3在马桑内酯所致癫痫大鼠海马Ca3区的表达变化。方法40只SD大鼠随机分为癫痫组30只(又分为3h、6h、24h三个亚组)和对照组10只,应用免疫组织化学方法检测海马神经元中Bcl-2、Caspase-3的表达。结果①Bcl-2于致痫后6h表达增加,并于24h减少,与对照组比较有显著性差异(p<0.05)。②Caspase-3于致痫后6h表达增加,并持续增加到24h,与对照组比较有显著性差异(p<0.05)。③致痫组Bcl-2与Caspase-3的表达成反比,差异有统计学意义(p<0.05)。结论Caspase-3蛋白的表达水平在癫痫发作后神经元的损伤中占有重要的作用,参与其凋亡的发生及其它功能的调控。Bcl-2可通过抑制Caspase-3的活性而抑制神经元的损伤,但是这种抑制作用是有限的。
Objective To explore the expression changes of Bcl-2 and Caspase-3 in hippocampus CA3 region of epileptic rats induced by Coriaria Lactone （CL）. Methods 40 rats were divided into epilepsy group which were divided into 3 hour subgroup, 6 hour subgroup and 24 hour subgroups （10 rats in each subgroup） ,and control group which included 10 rats. Bcl-2 and Caspase-3 were detected using immunohistochemical method. Results OThe expression of Bcl-2 was increased at 6 hour after CL-induced epilepsy and reduced at 24 hour, which was significantly different from the control group（p〈0. 05）. QThe expression of Caspase-3 was increased at 6 hour after CL-induced epilepsy and to 24 hour continuously, which was significantly different from the control group（p〈0. 05）. （1）The expression of Bcl-2 was inversely proportional to Caspase-3 in epilepsy group and the difference was statistically significant （p〈0.05）. Conclusion Caspase-3 plays a vital role in epilepsy-induced neuronal injury and regulates its apoptosis; Bcl-2 may relieve damage of neuron through suppressed the caspase-3 activity limitedly.
出处
《四川解剖学杂志》
2008年第1期5-7,共3页
Sichuan Journal of Anatomy
