摘要
目的 探讨长春西汀（Vinpocetine,Vinp）对脑卒中后抑郁（PSD）模型大鼠脑内单胺类递质的影响及治疗PSD的可能机理.方法 36只大鼠随机分为假手术组（n=8）、生理盐水组（n=10）、Vinp低剂量组（n=9）、Vinp高剂量组（n=9）,采用颈内动脉线栓法制备局灶性脑缺血大鼠模型并予以慢性不可预见的温和刺激制备PSD大鼠模型,在造模后分别给予Vinp（5m/kg,10mg/kg）的药物干预,生理盐水组以同样给药途径予等剂量的生理盐水,于第14,28天时进行行为学观察和测试,行为学观察完成后采用荧光检测法测定大鼠额顶皮层、海马和脑干区单胺类递质的变化.结果 复合造模处理可引起局灶性脑缺血大鼠模型体质量增长缓慢,大鼠敞箱实验水平活动得分、糖水消耗量都明显减少,强迫游泳不动时间明显增多,抑郁的行为学评分明显降低;而Vinp能提高抑郁的行为学评分,改善抑郁症状,并能显著增加PSD大鼠脑内NE、5-HT、DA水平,在大鼠额顶皮层、海马和脑干区,Vinp高剂量（10mg/kg）组分别为NE[（192.4±34.8）ng/g,（206.0±41.7）ng/g,（91.1±23.0）ng/g]、5-HT[（494.1±50.7）ng/g,（599.7±39.2）ng/g,（541.7±62.6）ng/g]、DA[（298.6±32.6）ng/g,（297.0±38.1）ng/g,（85.9±24.3）ng/g]较生理盐水组NE[（92.4±17.5）ng/g,（131.4±34.8）ng/g,（49.0±13.6）ng/g]、5-HT[（367.8±87.3）ng/g,（498.7±79.6）ng/g,（320.4±59.4）ng/g]、DA[（106.1±23.0）ng/g,（97.0±21.7）ng/g,（50.4±13.8）ng/g]明显增高,差异有显著性（P＜0.01）;且Vinp（10mg/kg）组大鼠脑内单胺类神经递质较（5mg/kg）组增高的幅度更大,提高抑郁的行为学评分更明显.结论 Vinp可以通过提高PSD大鼠的脑内单胺类递质水平而起到治疗PSD的作用.
Objective To observe the effect of vinpocetine on monoamine transmitters in cerebral of poststroke depression （PSD）rats and to investigate the mechanism of pharmacotherapeutics on PSD. Methods Rats were divided randomly into the sham-operated group,the normal saline group,the low dose of vinpocetine group and the high dose of vinpocetine group. Giving the left middle cerebral artery occlusion, the PSD rat model was established by unexpected chronic mild stress. When the PSD rat model was established, vinpocetine group was given vinpocetine（5mg/kg, 10mg/kg） and the normal saline group was given normal saline. Then the ethological score of depression was evaluated on 14 and 28 days. The monoamine transmitter in the frontal cortex and hippocampus and brainstem were detected by the fluorospectrophotometry. Results On the 28th day after the model establishment,compared with the normal saline group, the ethological score of depression level was decreased obviously. Compared with the normal saline group, vinpocetine could improve the ethological score of depression level of the PSD rat model, and these concentrations of 5-hydoxytrypatarmine （ 5-HT）, noradrenalin （ NE ） and dopamine （ DA ） in the frontal cortex, hippocampus and brainstem. The level of NE （ （ 192.4 ± 34.8 ） ng/g, （ 206. 0 ± 41.7 ） ng/g,（91.1 ±23.0） ng/g] ,5-HT（ （494. 1 ± 50.7） ng/g, （599.7 ± 39.2） ng/g, （541.7 ± 62.6） ng/g） and DA （ （ 298.6 ± 32.6） ng/g, （ 297.0 ± 38.1 ） ng/g, （ 85.9 ± 24.3 ） ng/g） in the high dose of vinpocetine group were significantly higher than that in the normal saline group （ NE （92.4 ± 17.5 ） ng/g, （ 131.4 ± 34.8 ） ng/g, （49.0 ±13.6）ng/g;5-HT（367.8 ±87.3） ng/g,（498.7 ± 79.6） ng/g, （320.4 ±59.4） ng/g; DA（ 106.1 ±23.0）ng/g,（97.0 ±21.7）ng/g, （50.4 ± 13.8 ）ng/g）（P 〈 0.01 ）. There were increased obviously by the high dose than the low dose of vinpocetine group. Conclusion Vinpocetine could treat PSD by increasing the level of monoamine transmitters in PSD rats＇ brain.
出处
《中华行为医学与脑科学杂志》
CAS
CSCD
北大核心
2011年第4期315-318,共4页
Chinese Journal of Behavioral Medicine and Brain Science
关键词
长春西汀
脑卒中后抑郁
大鼠
神经递质
Vinpocetine
Post-stroke depression
Rats
Neurotransmitter
