摘要
目的观察杏仁核点燃癫痫大鼠海马区P．糖蛋白（P—gp）表达及苔藓纤维出芽（MFS）的动态变化。方法90只大鼠采用随机数字表法分为假手术对照组（10只1、癫痫组（40只）和治疗组（40只），假手术对照组只安装电极，不予刺激；癫痫组和治疗组制作杏仁核点燃模型，治疗组加用左乙拉西坦灌胃治疗[100mg／（kg·d1，2次／d）1。采用Timm银染组织化学方法观察海马区MFS，免疫组化法检测P—gP的表达。结果f1）成功制造癫痫模型后，在海马CA3区透明层出现异常MFS．其中S1亚组大鼠MFS评分最低，与假手术对照组比较差异无统计学意义（p0．05）；S2亚组大鼠评分开始增高，S4亚组大鼠明显增高，s8亚组大鼠达到高峰，与假手术对照组比较差异均有统计学意义（P〈0．05）。而治疗组大鼠MFS评分各时间点与假手术对照组比较差异均无统计学意义（胗O．05）。（2）癫痫发作后癫痫组大鼠P．gp表达量呈现出逐渐降低的趋势，S1、S2、S4亚组与假手术对照组差异有统计学意义（P〈0．05）；S8亚组接近正常水平，与假手术对照组比较差异无统计学意义（P〈0．05）。治疗组大鼠除Y1亚组外，余各亚组P．gp表达量与假手术对照组比较差异均无统计学意义（p〈0．05）。结论MFS是慢性癫痫形成的重要机制，P．gP是癫痫发生的产物，是癫痫药物耐药的主要原因。
Objective To explore the relationship between plasticity of hippocampus neuronal morphology and pathogenesis of epilepsy by observing the changes of mossy fiber sprouting （MFS） and P-glycoprotein （P-gp） expression in the hippocampus of rat models of amygdala-kindling epilepsy. Methods Ninety male Wistar rats were randomly divided into epilepsy model group （n=40）, drug treatment group （n=40） and sham-operated group （n= 10）. Models of chronic epilepsy were established by stimulating the amygdale; rats in the drug treatment group were perfused antiepileptic drug levetiraeetam into stomach [100 mg/（kg.d）, twice daily]. At different observation time points （1, 2, 4 and 8 weeks after the treatment）, Timm staining was employed to observe the changes of MFS; immunohistochemical method was used to detect the dynamic changes of P-gp. Results （1） After the success of model making, abnormal MFS levels in the hippocampal CA3 transparent layer were noted; lowest MFS scores were noted in S1 subgroup, which showed no significant difference as compared with those in sham-operated group （P〉0.05）; the MFS scores in S2, S4 and S8 subgroups increased gradually with a peak level at 8 weeks after inducement, which showed significant difference as compared with those in sham-operated group （P〈0.05）. No significant differences on MFS grading scores were noted in the drug treatment group between each two time points （P〉0.05）. （2） The P-gp expression in the epilepsy model group showed significant difference at different time points （P〈0.05）; highest expression level was noted at one week after the surgery, and returned to normal at four weeks. However, the P-gp expressionshowed no significant difference in the drug treatment group between each two time points （P〉0.05）, except for 1 week after treatment. Conclusion MFS is the important mechanism of chronic epilepsy, and P-gp is the product of epilepsy, which is the main reason of epilepsy drug resistance.
出处
《中华神经医学杂志》
CAS
CSCD
北大核心
2013年第7期657-660,共4页
Chinese Journal of Neuromedicine
