A molecular biological study on resistance to brain damage induced by prolonged seizure in premature brain

JIANG Li; et al

doi:10.13406/j.cnki.cyxb.2005.05.003

您当前的位置：

首页 >

文章列表页 >

A molecular biological study on resistance to brain damage induced by prolonged seizure in premature brain

更新时间：2024-01-17

- A molecular biological study on resistance to brain damage induced by prolonged seizure in premature brain
- Journal of Chongqing Medical University Issue 5, (2005)
- 作者机构：
  
  1. 重庆医科大学附属儿童医院神经内科
  2. 重庆医科大学附属儿童医院神经内科,重庆,400014
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2005.05.003
  CLC： R742.1
- Published：2005，
扫描看全文
[1]蒋莉,蔡方成,张晓萍.未成熟大脑对惊厥性脑损伤耐受性的分子生物学机理研究[J].重庆医科大学学报,2005(05):14-17.

JIANG Li, et al. A molecular biological study on resistance to brain damage induced by prolonged seizure in premature brain. [J]. Journal of Chongqing Medical University (5).(2005)
[1]蒋莉,蔡方成,张晓萍.未成熟大脑对惊厥性脑损伤耐受性的分子生物学机理研究[J].重庆医科大学学报,2005(05):14-17. DOI： 10.13406/j.cnki.cyxb.2005.05.003.

JIANG Li, et al. A molecular biological study on resistance to brain damage induced by prolonged seizure in premature brain. [J]. Journal of Chongqing Medical University (5).(2005) DOI： 10.13406/j.cnki.cyxb.2005.05.003.

摘要

目的:探讨幼龄鼠未成熟脑组织对惊厥性脑损伤中细胞凋亡与坏死病理过程具有主动保护性抑制机制的分子生物学机理。方法:健康成年及幼龄Wistar鼠经皮下与腹腔内注射美解眠致惊。两组分别于严重惊厥发作后1、2、4、12、24、48、72h、7天时点上断头处死取脑

在进行组织病理学动态观察神经元坏死、凋亡的基础上

采用免疫组化法

原位检测脑片凋亡相关基因bcl-2、P53的表达变化

分别计算其弱、强阳性表达细胞数。结果:（1）严重惊厥后

成年鼠与幼鼠脑内P53和bcl-2的表达截然不同。成年鼠P53阳性表达率高达90%

其中一半属中、高度强阳性。但bcl-2表达率仅57%

且主要呈低度表达;相反

幼鼠以bcl-2强表达为主

其阳性表达率达85%以上。（2）动态观察获类似结果。严重惊厥后3天

成年鼠脑内仍有持续P53强表达

但其bcl-2于发作后仅数小时

已回落与对照无差异;相反

幼鼠则在发作3天内显示bcl-2的持续强表达

而P53于发作后12h开始明显降低

并于24h后与对照不再有差异。结论:持续惊厥发作后

未成熟及成熟期神经元中凋亡的诱导和抑制基因均同时表达

但两者间存在显著年龄差异。未成熟脑神经元中

以凋亡抑制基因bcl-2表达为主

而成熟脑神经元中凋亡诱导基因P53表达更显著。

Abstract

Objective:To explore the molecular biological base of internal protective response in premature brain which reduces the process of apoptosis and necrosis of neurons.Methods:Megimide was injected in healthy adult and baby rats(ARs & BRs) respectively to evoke prolonged seizures and status epilepticus(SE).ARs and BRs rats were sacrificed at 1

72 hours and 7 days after prolonged seizure stopped.Hippocampus

dentate gyrus and parietal cortex of their brain were taken for immunocytochemistry studies for apoptosis associated genes bcl-2 and P53 expression.Results:(1) There was a much stronger and higher rate(90%) of P53 expression in ARs’ brain

and such state continually kept even at 72h after seizure stopped;however bcl-2 expression was weak and low(57%)

and no difference was found in bcl-2 expression only several hours compared with normal control.(2) In BRs’ brain there was more than 85% neurons within a strongest expression of bcl-2;and the strongest bcl-2 expression sustained in 72h after SE

however P53 expression lasted less than 24h.Conclusion:Significant difference between premature and mature brain is shown on the genes’ expression associated apoptosis after seizure.Anti apoptosis gene(bcl-2) expression is much higher and longer than apoptosis gene(P53) in BRs’ brain

and it is reversed in ARs group.So the strongest expression of bcl-2 after SE could be the important molecular biological basis for the special resistance to neuron injury in premature brain.

关键词

惊厥脑损伤Wistar鼠Bcl-2p53

Keywords

SeizureBrain damageWistar ratsBcl-2p53

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

A novel antiapoptosis gene,survivin,expression in bladder transitional cell cancer

Expressions of p53 and bcl-2 in non-small-cell lung cancer

Clinical and pathological features of keratoacanthoma

Effect of Lingo-1 on axon with Mg²⁺-free-induced neuron seizure-like discharge

IL-17-JAK2/STAT3 signaling pathway reduces chemo-induced apoptosis in hepatocellular carcinoma through regulating p53

Related Author

HE Weiyang

et al

祝海洲

詹自力

DENG Hongbin

et al

刘宇

SHAN Kui

Related Institution

Department of Urology, College of Clinical Medicine, Chongqing Medical University

济宁医学院外总教研室

重庆医科大学临床学院泌尿外科

Department of Oncology , College of Clinical Medicine, Chongqing Medical University

⁰