关键词：
新生大鼠;反复惊厥;Cathepsin D;Caspase-3
摘 要：
将42只大鼠随机分为试验组和对照组,以吸入三氟乙醚诱导反复惊厥发作模型,采用RT-PCR法检测新生期反复惊厥大鼠海马神经元中溶酶体蛋白酶(Cathepsin)D与含半胱氨酸的天冬氨酸蛋白水解酶(Caspase)-3的表达,探讨其在反复惊厥后对脑损伤中的影响。结果表明:Cathepsin D在惊厥后0h即明显高于对照组,在惊厥后12h进一步增高(0.063 44±0.008 72、0.042 96±0.006 57,P<0.01),24h后与对照组比较差异不显著(P>0.05);与对照组相比,Caspase-3在惊厥后1.5h开始增高,在惊厥后12h显著增高(0.004 70±0.000 34、0.003 10±0.000 22,P<0.01),并持续至惊厥后24h,差异显著(P<0.05),48h后下降。说明反复惊厥增强了新生期大鼠海马神经元Cathepsin D、Caspase-3表达,Cathepsin D、Caspase-3可能参与反复惊厥后神经元损伤的病理过程。
译 名：
Recurrent seizures in neonatal rats:enhanced gene expression of Cathepsin D and Caspase-3 in hippocampal neurons
作 者：
LIU Yueying;TIAN Tian;LI Lili;CHEN Jieru;NI Hong;Affil Hosp,Jiangnan Univ;Chil Hosp Affil,Soochow Univ;
关键词：
neonatal rat;;recurrent seizures;;cathepsin D;;caspase-3
摘 要：
42rats were randomly divided into two groups(experimental group and control group)equally.Flurothyl was used to induce recurrent seizures in neonatal rats.The gene expression of Cathepsin D and Caspase-3in hippocampal neurons was detected by RT-PCR.This study aimed to investigate whether both genes were involved in neuronal damage after recurrent neonatal seizures or not.At 0h after final seizures,there was higher expression of Cathepsin D in experimental group than that in control group.At 12 hafter final seizures,the expression of Cathepsin D in experimental group(0.063 44±0.008 72)was further higher than that in control group(0.042 96±0.006 57),P<0.01;and at 24 hafter final seizures,there was no difference between experimental group and control group,P>0.05.The expression of Caspase-3in experimental group began to increase at 1.5hafter final seizures,and there was significant difference between experimental group and control group[(0.004 70±0.000 34)vs(0.003 10±0.000 22)]at 12 h,and as well as24 hafter final seizures,all P<0.05.After 48 h,there was no difference for the expression of Caspase-3between experimental group and control group,P>0.05.The results indicated that the expression of Cathepsin D and Caspase-3in hippocampal neurons was enhanced in recurrent neonatal seizures of rats,and both genes may be involved in the pathological process of neuronal damage after recurrent neonatal seizures.
