c-Jun氨基末端激酶信号通路在大鼠杏仁核电点燃癫痫模型的发病机制中的作用  

Role of C-Jun N-terminal kinase signal pathway in amygdala kindled rats

作　　者：刘平[1] 刘红朝[2,3] 李学慧[4] 王宝峰[5] 卢俊章[2,3] 吴俊[4] 陈旭[4] 舒凯[4] 

机构地区：[1]河南中医学院第一附属医院中医内科,郑州450000 [2]湖北省新华医院 [3]湖北中医药大学附属新华医院神经外科 [4]河南中医学院第三附属医院内科 [5]华中科技大学同济医学院附属同济医院神经外科

出　　处：《医药论坛杂志》2014年第5期7-9,共3页Journal of Medical Forum

基　　金：河南省科技攻关项目(102102310147)

摘　　要：目的观察大鼠杏仁核电点燃癫痫模型海马区的JNK水平及病理变化。方法将健康雄性wistar大鼠,随机分为空白对照组、手术对照组和点燃组。10次癫痫发作后灌注取脑,Western blot法检测JNK的表达,进行胶原纤维酸性蛋白(GFAP)和尼氏染色,各组间进行比较。结果 Western blot显示点燃组海马区的JNK磷酸化水平(0.537±0.050)较空白组(0.379±0.050)和手术对照组(0.387±0.043)显著增高(P<0.05),总JNK水平各组之间差异无统计学意义(P>0.05);点燃组GFAP阳性细胞计数(68.12±5.36)较空白组(39.83±3.90)和手术对照组(40.26±4.51)显著增加(P<0.05);尼氏染色阳性细胞计数点燃组(19.14±3.87)较空白对照组(43.15±5.62)手术对照组(42.91±4.25)显著减少(P<0.05)。结论 JNK信号通路可能参与颞叶癫痫海马硬化形成,表现为磷酸化JNK水平的升高。Objective To observethe change of C -Jun N · terminal kinase （JNK） phophorylation and the pathological changes of the hippocampus in amygdale kindled rats. Methods Thirty rats were randomly divided into three groups （n = 10 each） ： blank group （ KB）, sham control （ AB - C）, kindling group （KI））. Whole - cell extracts of tissues were obtained from the right hippoeampus, and Westem blotting was used to detect the changes of total JNK and phosphorylation of JNK. Pathological changes of the hippocampus were observed by GFAP slain and Nissl stain. Results The level of JNK phosphorylation in the hippocampus was significantly higher （ P 〈 0.05 ） in the KD （0. 537 ±0. 050） than the KB （0. 379 ±0. 050 ） and the AB - C （ 0. 387 ± 0. 043 ）. Expression of total JNK in the hippocampus remained unchanged in kindled rats compared with the sham control and blank group（ P 〉 0. 05 ）. The expression of GFAP in the hippocampus of KD （ 68. 12 ±5.36 ） was significantly stronger （ P 〈 0.05 ） than that in the KB （ 39. 83 ± 3.90） and the AB - C （ 40. 26 ± 4. 51 ）. Nissl stain positive cells in the hippocampus of the KD （19. 14 ± 3.87） were significantly less （P 〈0. 05 ）than those in the KB （43. 15± 5.62） and the AB - C （42. 91 ±4. 25 ）. Conclusion The role of repeated activation of JNK can be related to the hippocampal sclerosis in amygdala kindled rats. JNK signaling pathway may be a new target to inter- fere with the development of hippocampal sclerosis in the temporal lobe epilepsy.

关 键 词：c—Jun氨基末端激酶 颞叶癫痫 海马硬化 

分 类 号：R-332[医药卫生]