摘要
目的观察癫痫持续状态(SE)SD大鼠幼鼠的海马区神经细胞的凋亡与Caspase3和Caspase9的表达关系,研究鼠神经生长因子(NGF)对其干预作用。方法采用氯化锂-匹罗卡品方法制备幼鼠SE模型,用TUNNEL染色观察海马区神经细胞凋亡情况,用免疫组化法分别检测Caspase3和Caspase9的表达。结果正常组TUNNEL阳性细胞在各观察点仅少量表达,SE组在8 h明显增加,72 h达到高峰,NGF组表达基本同SE组,但对应时间点显著减少(除4 h外,P<0.05);Caspase3和Caspase9在正常组仅有少量表达,SE组在4 h仅少量增加,24 h达到高峰,NGF组Caspase3、Caspase9在SE后24 h及72 h较SE组显著减少(P<0.01)。结论 SE可致幼鼠海马区神经元凋亡,随时间增加神经元凋亡加重,Caspase3和Caspase9的激活加重神经细胞的凋亡;NGF可减轻神经细胞的凋亡。
Objective To explore the effect and mechanism of nerve growth factor （NGF） by testing the expression of Caspase3 and Caspase9 in the hippocampus of immature SD rats after status epilepticus （SE）. Methods Lithium - pilocarpine model of SE in immature SD rats were established. The apoptotic neuron was detected by TUNEL （TdT - mediated dUTP Nick End Labeling）, and the expression of Caspase3 and Caspase9 were detected by immunohistochemical method. Results In normal group, TUNNEL- positive cells, Caspase3 and Caspase9 expressed only a small amount at each time point. In SE group, the positive cells increased significantly at all observed points, and reached peak at 72 h. The positive cells in the NGF group reduced significantly at each time point （ except 4 h, P 〈 0.05）. Theexpression of activated Caspase3 and Caspase9 protein reached peak at 24 h. Compared with the SE group, the expression of acti- vated Caspase3 and Caspase9 protein revealed a decrease in the NGF group at 24 h and 72 h （P 〈 0. O1 ）. Conclusion SE may lead to rats hippocampal neuronal apoptosis, and the neuronal apoptosis increases with time. Activated Caspase3 and Caspase9 can aggravate neuronal apoptosis. NGF can reduce the apoptosis of nerve cell and protect the brian.
出处
《河南医学研究》
CAS
2016年第9期1539-1541,共3页
Henan Medical Research
