异丙酚对抑郁大鼠电休克治疗后海马神经元环氧化酶-2表达的影响  

作　　者：刘小滨[1] 闵苏[1] 罗洁[1] 刘超[1] 李炜[1] 李晓[1] 

机构地区：[1]重庆医科大学附属第一医院麻醉科,400016

出　　处：《中华麻醉学杂志》2012年第2期154-157,共4页Chinese Journal of Anesthesiology

基　　金：国家自然科学基金（30972831）,重庆市教育委员会科学技术研究项目资助项目计划（KJ090309）

摘　　要：目的 探讨导师丙酚对抑郁大鼠电休克治疗后海马神经元氧化毓-2（COX-2）表达的影响。方法 健康成年雄性SD大鼠50只，2-3月龄，体重200-500g，采用连续不可预见性慢性应激制备抑郁模型，造模成功的40只大鼠，采用随机数字表达，将其随机分为4组（n=10），抑郁组（D组），异丙酚组（P组）、电休克组（E组）和异丙酚联合电休克组（PE组），另取10只大鼠作为正常对照组（C组），P组和PE组腹腔注射异丙酚80mg/kg，其它3组给予等容量生理盐水，E组和PE组分别于给予生理盐水8mg/kg或异丙酚后5min时进行电休克治疗，1次/d，连续7d。分别于造型前、造模后和治疗结束后进行水迷宫实验，记录逃避潜伏期和目标象限游泳时间百分比。然后处死大鼠，取海马组织、检测COX-2表达。结果 与C组比较，D组、P组、E组和PE组造模后逃避潜伏期延长，目标象限游泳时间百分比降低，海马组织COX-2表达上调，D组、P组和E组治疗结束后逃避潜伏期延长，目标象限游泳时间百分比降低（P〈0.05）,与D组比较，E组治疗结束后逃避潜伏期延长，海马组织COX-2表达上调，PE组逃避潜伏期缩短，目标象限游泳时间百分比升高（P〈0.05）；与E组比较，PE组治疗结束后逃避潜伏期缩短，目标象限游泳时间百分比升高，马海组织COX-2表达下调（P〈0.05）, 结论 异丙酚可改善抑郁大鼠电休克治疗认知功能，其机制与下调海马神经COX-2表达有关。Objective To investigate the effect of propofol on cyclooxygenase-2 (COX-2) expression in hippocampal neurons in depressed rats after electroconvulsive therapy (ECT).Methods Fifty 2-3 months old male SD rats weighing 200-250 g were randomly divided into 5 groups (n =10 each):group control (group C) ; group depression (group D); group propofol (group P); group ECT (group E) and group propofol + ECT (group PE).Depression was induced by separation and chronic unpredictable mild stres in groups D,P,E and PE.Groups P and PE received intraperitoneal pro pofol 80 mg/kg.Groups E and PE received ECT at 5 min after IP normal saline 8 ml/kg and propofol 80 mg/kg respectively once a day for 7 consecutive days.The learning and memory function was assessed by using Morris water maze test before (baseline) and after depression was induced and ECT.The animals were then sacrificed and their brains removed for detection of COX-2 mRNA expression in hippocampus (by RT-PCR).Results In group D depression significantly prolonged evasive latency and decreased swimming time percentage in platform quadrant and up-regulated COX-2 mRNA expression as compared with group C.In group E ECT further prolonged evasive latency and up-regulated COX-2 mRNA expression in depressed rats.In group PE propofol pretreatment attenuated ECT-induced impairment of learning-memory function and increase in COX-2 mRNA expression as compared with group E.Conclusion Propofol can ameliorate the decrease in learning and memory function induced by ECT in depressed rats by inhibiting COX-2 expression in hippocampal neurons.

关 键 词：二异丙酚 抑郁症 电惊厥疗法 环氧化酶2 海马 

分 类 号：R614[医药卫生—麻醉学]