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Effects of Rongchang capsules on expression of brain-derived neurotrophic factor and its TrkB in hippocampus after pentylenetetrazol-induced epileptic seizure in rats
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DOI   10.11656/j.issn.1672-1519.2013.07.15
Key Words   epilepsy;Rongchang capsule;brain-derived neurotrophic factor;TrkB
Author NameAffiliationE-mail
YANG Chang-quan Department of Pediatrics, The First Affiliated Hospital of Tianjin University of TCM, Tianjin 300193, China  
MA Rong Department of Pediatrics, The First Affiliated Hospital of Tianjin University of TCM, Tianjin 300193, China ycq1975@yahoo.com.cn 
YAN Jing-rui Tianjin University of TCM, Tianjin 300193, China  
Abstract
    [Objective] To explore the effect of Rongchang capsules (RCC) on the expression of brain-derived neurotrophic factor (BDNF) and its TrkB in hippocampus after pentylenetetrazol-induced epileptic seizure in rats. [Methods] The 40 rats were randomly divided into normal group, model group, valproic acid sodium(VPA) group and RCC group. The model of epileptic rats was kindled by PTZ. We observed the frequence of epileptic seizures, levels, and the incubation period. Using RT-PCR method the expression level of BDNF and its TrkB in the hippocampus were detected.[Results] Compared with before treatment, the attack degree in treatment rats was reduced. Before modeling the number of attacks of each moled groups had no significant difference (P>0.05). After RCC treatment, the attack score was significantly decreased compared with model group. The onset score of each treatment groups was lower(P<0.05). There was no significant difference between RCC group and VPA group(P>0.05). The results of expression of BDNF in hippocampus tissue showed that the expression of BDNF mRNA in hippocampus tissue was significantly higher than the normal group, the Chinese medicine group and VPA group. The expression in Chnese medicine was increased significantly more than other groups (P<0.01). The trend of the expression of TrkB mRNA was the same as the expression of BDNF. [Conclusion] RCC can effectively control the attack frequency and level of the epilepsy and improve the ability of learning and memory of epilepsy in rats. The mechanism may be associated with the regulation of BDNF and TrkB expressions.

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