c-Jun氨基末端激酶抑制剂SP600125对杏仁核电点燃癫痫模型大鼠海马CA1区神经元的保护作用  

Protective action of SP600125,an inhibitor of c-Jun N-terminalk inase on hippocampal CA1 neuron in amygdala kindled epilepsy rats

作　　者：刘平[1] 刘红朝[2,3] 王宝峰[4] 谭一虎[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脑病二区,河南郑州450003 [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,湖北武汉430015 [4]华中科技大学同济医学院附属同济医院神经外科,湖北武汉430030

出　　处：《新乡医学院学报》2014年第11期889-891,895,共4页Journal of Xinxiang Medical University

基　　金：河南省科技攻关项目(编号:102102310147)

摘　　要：目的探讨c-Jun氨基末端激酶(JNK)抑制剂SP600125对杏仁核电点燃大鼠海马CA1区神经元的保护作用。方法将30只健康雄性Wistar大鼠随机分为点燃组、加药组及加药对照组,每组10只。大鼠10次癫痫发作后灌注取脑,Western blot法检测JNK和磷酸化JNK表达,进行胶原纤维酸性蛋白(GFAP)和尼氏染色,并将各组进行观察和比较。结果 Western blot显示加药组海马区JNK磷酸化水平(0.347±0.033)较点燃组(0.510±0.039)和加药对照组(0.476±0.045)显著降低,差异有统计学意义(P<0.05),总JNK水平各组间比较差异无统计学意义(P>0.05);加药组GFAP阳性细胞计数(42.27±4.63)较点燃组(68.82±5.36)和加药对照组(69.06±4.63)显著减少,差异有统计学意义(P<0.05);尼氏染色正常神经元计数加药组(37.82±6.30)较点燃组(19.87±3.58)和加药对照组(20.13±5.37)显著增加,差异有统计学意义(P<0.05)。结论 JNK特异性抑制剂SP600125对大鼠杏仁核电点燃癫痫模型CA1区海马神经元具有保护作用。通过SP600125抑制JNK的活性可能是治疗颞叶癫痫一种新的有效策略。Objective To explore the protective action of SP600125,an inhibitor of c-Jun N-terminalk inase（JNK） on hippocampal CA1 neuron in amygdala kindled rats. Methods Thirty health male Wistar rats were randomly divided into kindling group,medicine group and medicine control group,ten rats in each group. The brain tissue was obtained by perfusion after ten times epileptic seizure. Westem blotting was used to detect the expression of JNK and phosphorylation of JNK（ p-JNK）.Pathological changes of the hippocampus were observed by glial fibrillary acidic protein（GFAP） staining and Nissl staining and the results were compared in each group. Results The level of JNK phosphorylation in the hippocampus in the medicine group（0.347 ±0.033） was significantly lower than that in the kindling group（0. 510 ± 0. 039） and the medicine control group（0.476 ±0.045）（P〈0.05）. There were no statistic difference of the levels of total JNK in each group（P〉 0.05）. The positive cells of GFAP in medicine group（42. 27 ± 4. 63） were significantly lower than those in the kindling group（68. 82 ±5. 36）and the medicine control group（69. 06 ± 4. 63）（P〈0. 05）. Nissl staining showed that the number of normal neuron in the medicine group（37. 82 ± 6. 30） was significantly higher than that in the kindling group（19. 87 ± 3. 58） and the medicine control group（20. 13 ± 5. 37）（P〈0. 05）. Conclusion SP600125,a specific inhibitor of JNK,has a protective effect on neurons in hippocampal CA1 region in amygdala kindled model rats. SP600125 may be a new and effective strategy to treat temporal lobe epilepsy by suppressing the activation of JNK.

关 键 词：C-JUN氨基末端激酶 颞叶癫痫 海马硬化 SP600125 

分 类 号：R742.1[医药卫生—神经病学与精神病学]