摘要
目的探讨脑内氨基丁酸(γ-aminobutyric acid,GABA)转氨酶抑制剂丙戊酸钠(Sodium Valproate,简写为SV)对戊四唑(Pentylentetrazol,PTZ)诱导的大鼠癫痫模型的作用。方法健康SD大鼠38只,随机分为5组,对照组、癫痫组和SV低中高3个剂量组(5、10、20 mg/kg)。观察大鼠腹腔注射PTZ前后癫痫发作的情况,按Racine分级标准记录,同时记录皮层脑电图(ECoG),观察癫痫样放电的潜伏期及1小时内癫痫样放电活动持续时间。应用Western blot电泳分析海马内CA1区P38MAPK及其上游MKK3,下游c-MYC相关蛋白的表达。结果对照组给PTZ后均出现癫痫发作,程度均为5级,丙戊酸钠组发作程度明显减轻。ECoG潜伏期延长,痫样放电1小时持续时间缩短。同时,与对照组相比,癫痫组和SV 3个剂量组大鼠CA1区蛋白表达强度升高(P<0.05);与癫痫组相比,SV 3个剂量组大鼠CA1区蛋白表达强度降低(P<0.05)。结论 SV对PTZ诱导的癫痫大鼠的发作有明显的对抗作用,对癫痫大鼠海马具有保护作用,其作用与P38MAPK通路相关蛋白的表达相关。
Objective Explore the activation of P38MAPK in the PTZ-induced rats and effect of γ-aminobutyric acid receptor blocker Sodium Valproate.Methods 38 healthy SD rats were randomly divided into 5 groups,control group,epilepsy group and 3 different dose SV group（5mg/kg,10mg/kg,20mg/kg,respectively）.Observe seizures situation of rats before and after intraperitoneal injection,according to racine classification standard record,while recording cortical EEG（electrocoti-cogram,ECoG）,observe the incubation period of epileptiform discharges and epileptiform discharge duration within one hour.Analysis the expression of P38MAPK in CA1 area,of hippocampus.Expression of P38MAPK,upstream MKK3 and MYC-related protein were detected by Western blot.Results Epilepsy group all have seizure emerged after PTZ,the degree was 5,the degree of attack significantly reduced in the 3 SV groups.Incubation period of ECoG extended,the duration of one hour epileptiform discharges shorted.At the same time,compared with the control group,intensity of protein expression in CA1 area of rats increased in epilepsy group and 3 doses SV groups（P〈0.05）.Compared with the epilepsy group,intensity of protein expression in CA1 area of rats decreased in 3 doses SV groups（P〈0.05）.Conclusion SV has protective effet to PTZ-induced epileptic rats by depression of expression of P38MAPK-associated protein.
出处
《辽宁医学院学报》
CAS
2012年第1期19-22,共4页
Journal of Liaoning Medical University (LNMU) Bimonthly
关键词
癫痫
丙戊酸钠
皮层脑电图
epileptic
Sodium Valproate（SV）
electrocoti cogram
