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作 者:刘月影[1,2] 田甜[2] 李丽丽[2] 陈洁如[2] 倪宏[2]
机构地区:[1]江南大学附属医院,江苏无锡214062 [2]苏州大学附属儿童医院,江苏苏州215003
出 处:《扬州大学学报(农业与生命科学版)》2016年第2期22-25,共4页Journal of Yangzhou University:Agricultural and Life Science Edition
基 金:国家自然科学基金资助项目(81471337);无锡市卫生和计划生育委员会科研项目(MS201518)
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。42 rats 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-3 in hippoeampal 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 0 h after final seizures, there was higher expression of Cathepsin D in experi- mental group than that in control group. At 12 h after 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 h after final seizures, there was no difference between experimental group and control group, P〈0.05. The expression of Caspase-3 in experimental group began to increase at 1.5 h after final seizures, and there was significant difference between experimental group and control groupE(0. 004 70±0. 000 34) vs (0. 003 10±0. 000 22)] at 12 h, and as well as 24 h after final seizures, all P〈0.05. After 48 h, there was no difference for the expression of Caspase-3 between experi- mental group and control group, P〉0.05. The results indicated that the expression of Cathepsin D and Caspase-3 in hip- pocampal 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.
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