Effect of Chaihu Shugan Tang on excitability in different brain regions of pentylenetetrazole-kindled chronic epileptic rats.
- Author:
Wei XIE
1
;
Yunhong YU
;
Yunyan ZHAO
Author Information
- Publication Type:Journal Article
- MeSH: 4-Chloro-7-nitrobenzofurazan; analogs & derivatives; metabolism; Animals; Aspartic Acid; metabolism; Brain; drug effects; metabolism; physiopathology; Chronic Disease; therapy; Deoxyglucose; analogs & derivatives; metabolism; Disease Models, Animal; Drugs, Chinese Herbal; administration & dosage; Epilepsy; chemically induced; drug therapy; metabolism; physiopathology; Glutamic Acid; metabolism; Hippocampus; drug effects; physiopathology; Humans; Kindling, Neurologic; drug effects; Male; Pentylenetetrazole; administration & dosage; adverse effects; Random Allocation; Rats; Valproic Acid; metabolism
- From: China Journal of Chinese Materia Medica 2010;35(12):1619-1622
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of the Chinese compound prescription Chaihu Shugan Tang (CHSGT) on the excitability in the cerebral cortex and hippocampus (different brain regions) of pentetrazole (PTZ)-kindled chronic epileptic rats.
METHODTo establish the model of chronic kindling rats intraperitoneal injected with pentylenetet. Fully kindled rats were randomized into control and experimental groups for intragastric administration of normal saline (control, model), Sodium Valproate and CHSGT at the high, medium and low doses for 4 consecutive weeks. The content of 2-NBDG, the glutamate (Glu) and the aspartate (Asp) in different brain regions of rats were detected by fluorescence imaging techniques and HPLC assay respectively.
RESULTCHSGT at the high, medium and low doses all significantly decreased the content of 2-NBDG, the Glu and the Asp in different brain regions of chronic epileptic rats (P < 0.01).
CONCLUSIONCHSGT can inhibit the excitability in different brain regions of PTZ-induced epileptic rats, by decreasing the level of excitatory neurotransmitter maybe one of its antiepileptic mechanisms.