异丙酚麻醉对电休克诱发抑郁大鼠海马Tau蛋白过度磷酸化的影响  

Effect of propofol anesthesia on electroconvulsive therapy-induced hyperphosphorylation of Tau protein in hippocampus in depressed rats

作　　者：刘超[1] 闵苏[1] 刘东[2] 董军[1] 罗洁[1] 黎平[1] 刘小滨[1] 

机构地区：[1]重庆医科大学附属第一医院麻醉科,400016 [2]天津医科大学第二医院神经外科

出　　处：《中华麻醉学杂志》2012年第3期295-297,共3页Chinese Journal of Anesthesiology

基　　金：基金项目：国家自然科学基金（30972831）

摘　　要：目的探讨异丙酚麻醉对电休克诱发抑郁大鼠海马Tau蛋白过度磷酸化的影响。方法选取Open—field测试总分为30～120分的雌性WKY大鼠32只，24周龄，体重200～250g，采用随机数字表法，将其随机分为4组（n=8）：对照组（c组）、异丙酚组（P组）、电休克组（E组）和异丙酚＋电休克组（PE组）。c组腹腔注射生理盐水5ml；P组腹腔注射100mg／kg异丙酚5ml；E组腹腔注射生理盐水5ml，15min后施行电休克治疗；PE组腹腔注射100mg／kg异丙酚5ml，15min后施行电休克治疗。电休克治疗结束24h时，采用Morris水迷宫测定大鼠认识功能。认知功能测试完毕6h时，处死大鼠，取海马组织，检测磷酸化Tau蛋白的表达。结果与C组比较，P组、E组和PE组逃避潜伏期延长，游泳时间缩短，P组海马磷酸化Tau蛋白表达下调，E组海马磷酸化Tau蛋白表达上调（P〈0．05），PE组海马磷酸化Tau蛋白表达差异无统计学意义（P〉0．05）；与E组比较，PE组逃避潜伏期缩短，游泳时间延长，海马磷酸化Tau蛋白表达下调（P〈0．05）。结论异丙酚麻醉改善电休克诱发抑郁大鼠认知功能障碍的机制与抑制海马Tau蛋白过度磷酸化有关。Objective To investigate the effect of propofol anesthesia on electroconvulsive therapy （ECT）- induced hyperphosphorylation of Tau protein in hippocampus in depressed rats. Methods Thirty-two female WYK rats in which the total score was 30-120 after Open-field test, aged 24 weeks, weighing 200-250 g, were randomly divided into 4 groups （n = 8 each）： control group （group C）, propofol group （group P）, ECT group （group E） and propofol ＋ ECT group （group PE）. In groups C and E, the animals received intraperitoneal normal saline 5 ml, and in addition the animals received ECT 15 min later in group E. In groups P and PE, the animals received intraperitoneal 100 mg/kg propofol 5 ml, and in addition the animals received ECT 15 min later in group PE. The learning and memory function was assessed by Morris water maze test at 24 h after ECT. The animals were sacririced at 6 h after Morris water maze test and the hippocampal tissues were removed for determination of the expression of phosphorylated Tau protein . Results Compared with group C, the escape latency was significantly prolonged, the swimming time was significantly shortened in groups P, E and PE, the expression of phosphorylated Tau protein in hippocampus was down-regulated in group P, and the expression of phosphorylated Tau protein in hippocampus was up-regulated in group E （P 〈 0.05）. Compared with group E, the escape latency was significantly shortened, the swimming time was significantly prolonged, and the expression of phosphorylated Tau protein in hippocampus was down-regulated in group PE （ P 〈 0.05）. Conclusion The mechanism by which propofol anesthesia improves cognitive impairment induced by ECT may be related to inhibition of hyperphosphorylation of Tau protein in hippocampus in depressed rats.

关 键 词：二异丙酚 电惊厥疗法 抑郁 TAU蛋白质类 海马 

分 类 号：R614[医药卫生—麻醉学]