The effect of low-frequency transcranial magnetic stimulation pretreatment on seizures, the expression of B
10.3760/cma.j.issn.0254-1424.2011.07.003
- VernacularTitle:低频重复经颅磁刺激预处理对氯化锂-匹鲁卡品致痫大鼠痫性发作及B细胞淋巴瘤/白血病基因-2、自杀因子和半胱氨酸天冬氨酸蛋白酶-3蛋白表达的影响
- Author:
Sha KE
;
Hongning ZHANG
;
Junqiang ZHANG
;
Xiaoming WANG
;
Xiaoqiong ZHAO
;
Hui HUANG
;
Jianxiu HU
- Publication Type:Journal Article
- Keywords:
Transcranial magnetic stimulation;
Epilepsy;
B cell lymphoma;
B cell leukemia;
Fas protein;
Caspase-3
- From:
Chinese Journal of Physical Medicine and Rehabilitation
2011;33(7):488-493
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the possible mechanisms by which repetitive transcranial magnetic stimulation (rTMS) pretreatment antagonizes seizures induced by lithium chloride-pilocarpine and any correlation with antiapoptosis in hippocampal CA1 neurons.Methods Thirty rats were randomly divided into a control group, a sham stimulation group and an rTMS pretreatment group. The rTMS pretreatment group was pretreated on 7 consecutive days with low-frequency rTMS (0.5 Hz, 75％ of threshold intensity, 20 times/bundle, and 5 bundles/d), while the sham-stimulation group was sham-stimulated with a similar sound. Lithium chloride-pilocarpine ( LPC ) was used to induce a model epileptic state.Epileptic stroke latency and severity were recorded ; neuronal morphology was observed using hematoxylin and eosin (HE) staining; mean positive-reactive cell number and mean optical density and absorbance of B cell lymphoma/leukemia gene-2 (Bcl-2) were recorded, and Fas and Caspase-3 protein in the hippocampal CA1 region were observed with immunohistochemistry.Results Compared with the sham stimulation group, epileptic latency in the rTMS pretreatment group was significantly longer. Seizures in the rTMS pretreatment group were less severe, and a number of degenerated neurons were observed to be apoptotic. Bcl-2 protein expression increased at each time point, but Fas and Caspase-3 protein expression decreased.Conclusions rTMS pretreatment has an anti-epilepsy effect. The possible neuronal protection might be produced by regulating the expression of Bcl-2, Fas and Caspase-3 protein in the hippocampus.
