Your browser doesn't support javascript.
loading
Study on neuron apoptosis in the patients with temporal lobe epilepsy characterized by hippocampus sclerosis / 中国医师进修杂志
Chinese Journal of Postgraduates of Medicine ; (36): 10-12, 2014.
Artigo em Chinês | WPRIM | ID: wpr-467010
ABSTRACT
Objective To explore the role and expression of cell apoptosis regulatory genes in patients with temporal lobe epilepsy characterized by hippocampus sclerosis.Methods The experimental specimens were obtained from 15 patients with temporal lobe epilepsy (epilepsy group) and 6 control samples (control group) were obtained from temporal lobe excision of brain trauma decompression,investigated neuron apoptosis by HE stain,TdT-mediated dUTP-biotin nick end labeling (TUNEL) method,and determined the expression of bcl-2,bax and caspase-3 by immunohistochemistry.Results The evidence of neuron apoptosis was not found by HE stain in both control group and epilepsy group.Positive cells was not found in control group,but was obviously observed in epilepsy group by TUNEL staining [(4.39 ± 2.04) numbers/100].Unlike that in normal adult brain,bcl-2 immunoreactivity was obviously observed in some neurons in epilepsy group[(6.72 ± 3.36) numbers/100] (P < 0.01).Compared with control group,bax protein in epilepsy group was mild expression (P > 0.05).Two cases in control group were detected the expression of caspase-3 protein,and caspase-3 significantly increased in epilepsy group [(1.07 ± 0.43),(9.54 ± 3.68) numbers/100] (P < 0.01).Conclusions Neuron apoptosis is an important cause of hippocampal sclerosis of human epilepsy.bcl-2 and caspase-3 may play an important role in this process.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Postgraduates of Medicine Ano de publicação: 2014 Tipo de documento: Artigo

Similares

MEDLINE

...
LILACS

LIS

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Postgraduates of Medicine Ano de publicação: 2014 Tipo de documento: Artigo