Dynamic changes of kinesin family member 17 protein expression in the pilocarpine-induced rat model
10.3760/cma.j.issn.1006-7876.2013.08.004
- VernacularTitle:锂-匹罗卡品致痫大鼠脑组织中驱动蛋白家族成员17的表达情况
- Author:
Xiunan YU
;
Xueying ZHOU
;
Xingang LI
;
Shengnian ZHOU
- Publication Type:Journal Article
- Keywords:
Epilepsy,temporal lobe;
Kinesin;
Pilocarpine;
Disease models,animal
- From:
Chinese Journal of Neurology
2013;46(8):519-523
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the kinesin family member 17 (KIF17) expression and cellular localization in the hippocampus and temporal lobe cortex in the rat lithium-pilocarpine model of epilepsy,and discuss its function in the epilepsy pathogenesis.Methods The animal model was established by lithiumpilocarpine induction in rats.Totally 49 adult healthy male Wistar rats were randomly divided into control group (n =7) and experimental group (n =42).The experimental group included 6 subgroups (n =7)according to sacrifice time (24 h,72 h,7 d,14 d,1 month and 2 months).The expression and localization of KIF17 were examined by western blot and double-label immunofluorescence,respectively.Results In rat hippocampus,the expression of KIF17 protein increased after the onset of seizure (the ration of KIF17/β-actin were:24 h 0.516 ± 0.196,72 h 0.742 ± 0.313),reached its peak in 7 days (0.888 +0.319)and then slowed down (14 d 0.770 ± 0.271,1 month 0.742 ± 0.261,2 months 0.714 ± 0.271),all of which were significantly higher than that in the control group (0.495 ± 0.203).And all the differences had statistical significance (t =7.051,4.974,7.419,8.795,8.264,6.676,all P ＜ 0.05).In rat cortex of temporal lobe,the expression of KIF17 protein increased after the onset of seizure and reached its peak in 30 d.The optical density ration in the experimental groups were higher than that in the control group.Doublelabel immunofluorescence disclosed that the KIF17 localized in the neurons,including excitable neurons and inhibitory neurons,but not in the astrocytes which were performed with anti-microtubule-associated protein 2,anti-brain-specific Na-dependent inorganic phosphate cotransporter,anti-glutamate decarboxylase 1 and anti-glial fibrillary acidic protein,respectively.Conclusion KIF17 may play a potential role in the pathogenetic mechanisms of the rat lithium-pilocarpine model of epilepsy.
