摘要
目的探讨慢性不可预见性应激抑郁模型大鼠大脑皮层亚细胞成分蛋白激酶CβⅡ(PKCβⅡ)的表达水平以及三环类抗抑郁剂(TCAs)阿米替林、5-羟色胺再摄取抑制剂(SSRI)氟西汀对其影响。方法24只Sprague-Dewley雄性大鼠随机分为抑郁模型组6只,阿米替林治疗组6只,氟西汀治疗组6只,正常对照组6只。采用慢性轻度不可预见性应激方法建立抑郁模型,将9种刺激随机安排到18d,每天1种,应激前以及应激18d末对各组大鼠进行敞箱实验及液体消耗实验,第19天起阿米替林组、氟西汀组分别每天腹腔注射阿米替林(10mg.kg-1.d-1)、氟西汀(10mg.k-g1.d-1)1次,模型组及对照组每天腹腔注射等体积生理盐水1次,均持续21d。用蛋白质免疫印迹法检测大鼠大脑皮层亚细胞成分PKCβⅡ的表达水平。结果抑郁大鼠大脑皮层细胞膜PKCβⅡ蛋白表达水平(230.57±62.86)较对照组(331.26±17.94)明显减少(P<0.05);抑郁大鼠大脑皮层细胞浆PKCβⅡ蛋白表达水平(286.43±56.92)与对照组(343.55±70.48)比较,有下降趋势,但差异无显著性(P>0.05)。阿米替林、氟西汀治疗3周后抑郁大鼠大脑皮层亚细胞成分PKCβⅡ表达水平无明显变化(P>0.05)。结论大脑皮层细胞膜PKCβⅡ蛋白表达水平明显下降可能是抑郁症发病的重要环节。阿米替林、氟西汀对抑郁大鼠大脑皮层亚细胞成分PKCβⅡ的蛋白表达水平没有影响。
Objective To investigate protein kinase CβⅡ （ PKCβⅡ ） expression in subcellular fractionsfrom stress-induced depression rat brain and the effect of amitriptyline and fluoxitine on PKCβⅡ. Methods Twenty-four male Sprague-Dawley rats were randomly allocated to four groups： depression model, amitriptyline-treated , fluoxitine- treated and control group. Rats were exposed to unpredictable sequence of mild stressors. The ex-pression of PKCβⅡ was determined with Western blotting. Results The expression of membrane-associated PKCβⅡ in model group （230.57±62.86） was significantly lower than that in control group（331.26 ±17.94, P〈0.05 ）. It had a lower tendency to cytosol -associated PKCβⅡ in model group （286.43±56.92）than that in control group. Statistically, however, significant difference wash＇ t observed（ P 〉 0.05 ）. After 3-week paroxetine oramitriptyline treatment,it hash＇ t changed in the expression of PKCβⅡ in subcellular fractions from depression rat brain（ P〉 0.05）. Conclusion It is suggested that PKCβⅡ play an important role in the pathogenesis of depression. Amitriptyline or fluoxetine treatment doesn＇ t change the expression of PKCβⅡ in subcellular fractions from depression rat brain.
出处
《中国行为医学科学》
CSCD
2005年第8期678-680,共3页
Chinese Journal of Behavioral Medical Science
基金
辽宁省科委自然科学基金资助项目(002063)
