Academic Journal

Nuclear Factor-Kappa B Activity Regulates Brain Expression of P-Glycoprotein in the Kainic Acid-Induced Seizure Rats

التفاصيل البيبلوغرافية
العنوان: Nuclear Factor-Kappa B Activity Regulates Brain Expression of P-Glycoprotein in the Kainic Acid-Induced Seizure Rats
المؤلفون: Nian Yu, Qing Di, Hao Liu, Yong Hu, Ying Jiang, Yu-kui Yan, Yan-fang Zhang, Ying-dong Zhang
المصدر: Mediators of Inflammation, Vol 2011 (2011)
بيانات النشر: Wiley, 2011.
سنة النشر: 2011
المجموعة: LCC:Pathology
مصطلحات موضوعية: Pathology, RB1-214
الوصف: This study was aimed to investigate the effect of NF-κB activity on the seizure susceptibility, brain damage, and P-gp expression in kainic acid- (KA-) induced seizure rats. Male SD rats were divided into saline control group (NS group), KA induced epilepsy group (EP group), and epilepsy group intervened with NF-κB inhibitor-pyrrolidine dithiocarbamate salt (PDTC group) or with dexamethasone (DEX group). No seizures were observed in the rats of NS group. Compared with NS group, increased P-gp expression and NF-κB activation in the rat brain of the EP group were observed after KA micro-injection. Both PDTC and DEX pre-treatment significantly increased the latency to grade III or V seizure onset compared to EP group but failed to show neuron-protective effect as the number of survival neurons didn't significantly differ from that in EP group. Furthermore, PDTC pre-treatment significantly decreased P-gp expression along with NF-κB activation in the hippocampus CA3 area and amygdala complex of rats compared with the EP group, implying that NF-κB activation involved in the seizure susceptibility and seizure induced brain P-gp over-expression. Additionally, DEX pre-treatment only decreased P-gp expression level without inhibition of NF-κB activation, suggesting NF-κB independent pathway may also participate in regulating seizure induced P-gp over-expression.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 0962-9351
1466-1861
Relation: https://doaj.org/toc/0962-9351; https://doaj.org/toc/1466-1861
DOI: 10.1155/2011/670613
URL الوصول: https://doaj.org/article/25fd7098977043bc99b2316a1fab110c
رقم الانضمام: edsdoj.25fd7098977043bc99b2316a1fab110c
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:09629351
14661861
DOI:10.1155/2011/670613