摘要
目的:研究马桑内酯(CoriariaLactone,CL)对神经元微丝F-actin的影响及其与缝隙连接通道的关系,以及它们在癫痫发病中的意义。方法:利用培养的神经元,采用直接免疫荧光法,用激光扫描共聚焦显微镜观察细胞骨架F-actin的结构及分布,同时测定F-actin含量。结果:致痫剂量的马桑内酯作用于神经元48h后,F-actin的荧光强度较对照组降低(P<0.01),给予CL+1-庚醇(1-hepatal),CL+1-庚醇+丙戊酸钠,CL+1-庚醇+卡马西平作用于神经元48h后F-actin的荧光强度较对照组明显升高(P<0.01),且以加丙戊酸钠和卡马西平组更显著。结论:CL可引起细胞内F-actin含量的降低,而通道阻滞剂1-庚醇,抗癫痫药丙戊酸钠、卡马西平可引起细胞内F-actin含量的增加,这种变化影响细胞骨架微丝装配和神经元胞间信号传导,可能在癫痫的产生中发挥重要作用。
Objective:To observe the effecof Coriaria Lactone on the neurons'F-actin and it's relation with the gap junction, their significance in the epileptogenesis.Methods:Observing the structure and distribution of F-actin with the immunofluorescence and the laser scanning cofocal microscope,and measuring the relative fluorescent intensive of F-actin.Results:After the effect of CL on the neurons of 48 hours,the F-actin's relative fluorescent intensive is lower than the control group(P<0.01),while the effect of CL and 1-hepatal, CL and 1-hepatal and sodium valproate,CL and 1-hepatal and carbamazepine on the neuron of 48 hours,the F-actin's relative fluorescent intensive is higher than the control group(P<0.01),and the increase of the F-actin's relative fluorescent is more significant in the group which add sodium valproate or carbamazepine.Conclusions:CL can induce the decrease of the content of the neuron's F-actin,while the gap junction blocker(1-hepatal),the antiepileptic drugs(sodium valproate,carbamazepine)can increase it.These change may affect the assembly of the neurofilament and the signal conduction between the neurons,which may have an important role in the origin of the epilepsy.
出处
《华西医学》
CAS
2005年第2期291-292,共2页
West China Medical Journal
