目的:观察miR-132、miR-146a在内侧颞叶癫痫(mesial temporal lobe epilepsy,MTLE)患儿及幼年大鼠模型海马组织中的表达变化。方法:收集MTLE患儿海马标本及正常对照人海马标本,Real-time PCR方法检测两组人海马组织中miR-132、miR-146a的表达改变。利用匹罗卡品诱导建立幼年大鼠MTLE模型,收集急性期(造模后2 h)、潜伏期(造模后3周)、慢性期(造模后8周)海马组织标本及相应时间点对照组大鼠海马标本,Real-time PCR方法检测各实验组大鼠海马组织中miR-132、miR-146a的表达改变。结果:miR-132、miR-146a在患儿MTLE海马组织中表达明显升高,分别为2.2±0.1和3.0±0.2,与正常对照组(1.0±0.2)比较差异有统计学意义(P〈0.05)。miR-132在MTLE大鼠模型急性期、潜伏期及慢性期表达均明显增加,分别为5.2±0.5,2.5±0.2和3.6±0.2,较正常对照组大鼠(1.0±0.1)差异有显著性(P〈0.05);miR-146a在MTLE大鼠急性期改变不明显,在潜伏期及慢性期表达明显增加(2.8±0.2,1.8±0.2),与对照组大鼠(1.0±0.1)比较差异有统计学意义(P〈0.05)。结论:miR-132、miR-146a在MTLE患儿及幼年大鼠模型中存在差异表达,其可能与MTLE中脑组织炎症反应的异常调控有关。
Objective:To investigate the expressions changes of miR-132 and miR-146 a in hippocampal tissues in the children with mesial temporal lobe epilepsy( MTLE) and young rats model of MTLE.Methods:Firstly,we obtained the hippocampi from children with MTLE and normal control.Real-time PCR was used to detect the expressions of miR-132 and miR-146 a.Secondly,young rats model of MTLE was induced by chloride lithium-pilocarpine.Expression changes of miR-132 and miR-146 a were monitored by Real-time PCR method in the acute,latent,and chronic stages of disease( 2h,3 weeks and 8 weeks after induction of lithium-pilocarpine status epilepticus,respectively),and in control hippocampal tissues corresponding to the same time points.Results:Both miR-132 and miR-146 a showed significant upregulation( P〈0.05) in hippocampal tissues of MTLE children( 2.2 ± 0.1 and 3.0 ± 0.2) compared to control group( 1.0 ±0.2).And miR-132 was upregulated significantly in the three stages( P〈0.05) in MTLE rats model( 5.2 ± 0.5,2.5± 0.2 and 3.6 ± 0.2,respetively) compared to their control groups( 1.0 ± 0.1).Though change of miR-146 a was notobviously in the acute stage,but it increased significantly( P〈0.05) in the latent and chronic stages( 2.8 ± 0.2 and1.8 ± 0.2) compared to control groups( 1.0 ± 0.1).Conclusion:There were great differences in the expression patterns of miR-132 and miR-146 a in both MTLE children and young rats model.These maybe was involved in the dysregulation of brain inflammations during MTLE development.