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舒必利对抑郁大鼠模型脑内酶的影响 被引量:5

Sulpiride effect on the enzyme activeness in the brain of model rat with depressive disorder
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摘要 目的:研究抑郁症模型大鼠脑内单胺氧化酶(MAO)、谷胱甘肽硫转移酶(GST)、γ-谷胺酰转移酶(γ-GT)的活性改变,探讨舒必利治疗抑郁症的作用机制。方法:本实验分为正常对照组、抑郁症模型组和舒必利治疗组3个实验组,每组10只Wistar雄性大鼠,除正常对照组外,其余两组均单笼饲养。从第14日起,抑郁症模型组和舒必利治疗组的大鼠按程序给予刺激,同时,抑郁症模型组的大鼠每日腹腔注射生理盐水1.0ml,舒必利治疗组的大鼠每日腹腔注射舒必利32.5mg/kg,在刺激的前、中、末期,分别对每只大鼠进行行为学测定和糖水消耗实验。刺激进行27d后,处死大鼠,冰上取脑,检测各实验组大鼠脑内MAO、GST、γ-GT的活性。结果:抑郁症模型组的MAO较正常对照组显著增高(P<0.05),舒必利治疗组与正常对照组间的差异无显著性(P>0.05);抑郁症模型组的γ-GT的活性较正常对照组和舒必利治疗组显著增高(P<0.01),正常对照组与舒必利治疗组间无显著差异(P>0.05);GST的活性在各组间均无显著差异。结论:舒必利治疗抑郁症模型大鼠可引起MAO、γ-GT的活性降低。 Objective: To study the enzyme activeness changes of monoamine oxidase (MAO), glutathione S- transferase (GST) and γ-glutamyl transferase (γ-GT) in depressive disorder model rat' s brain and explore the mechanism of sulpiride treatment in rats with depressive disorder. Method: 30 Wistar rats were divided into normal-controlled group,depressive disorder group and sulpiride-treated group. Except the normal-controlled group, the rest two groups were monocage bred. From the fourteenth day, the rats of dispressive disorder group and sulpiride-treated group were given routine programme stimula, meanwhile, saline 1.0 ml/kg and sulpiride 32.5 mg/kg were given into the rats every day by intraperitoneal injection respectively. At the prophase, metaphase and anaphase of the stimula, every rat was carried out ethology determination and sugar consumption experiment. 27 days after the stimula, all the rats were executed, their brains taken out on the ice and MAO, GST and γ-GT enzyme activeness detected. Results: The level of MAO activeness in depression disorder group was significantly higher than level of MAO in normal-controlled group ( P 〈 0.05) ,but significant difference didn't exist between normal-controlled group and sulpiride-treated group ( P 〉 0.05). The level of γ-GT in depression disorder group was significantly higher than that of normal-controllod group and sulpiride-treated group ( P 〈 0.01),however,there was no difference in the level of γ-GT between normal-controlled group and sulpiride-treated group ( P 〉 0.05) .There was no significant difference in the level of GST activeness between the three groups. Collusion: Sulpiride treatment in the depressive disorder model rats can lower the enzyme activeness of MAO and γ-GT.
出处 《临床精神医学杂志》 2007年第1期13-15,共3页 Journal of Clinical Psychiatry
基金 黑龙江省卫生厅资助项目(2004-032)
关键词 舒必利 抑郁 单胺氧化酶 谷胱甘肽硫转移酶 γ-谷胺酰转移酶 sulpiride depression monoamine oxidase glutathione S-transferase γ-glutamyl transferase
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参考文献9

  • 1Katz RJ,Roth KA,Carroll BJ.Acute and chronic stress effects on open field activity in the rat:implications for a model of depression[J].Neurosci Biobehav Rev,1981,5:247-251.
  • 2Willner P,Towell A,Sampson D,et al.Reduction of sucrose preference by chronic unpredictable mild stress,and its restoration by a tricyclic antidepressant[J].Psychopharmacology,1987,93:358-364.
  • 3Robinson DS.Monoamine oxidase inhibitors:a new generation[J].Psychopharmacol Bull,2002,36:124-138.
  • 4Du L,Faludi G,Palkovits M,et al.High activity-related allele of MAOA gene associated with depressed suicide in males[J].Neuro Report,2002,13:1195-1198.
  • 5Wells DG,Bjorksten AR.Monoamine oxidase inhibitors revisited[J].Can J Anaesth,1989,189:3664-3674.
  • 6金光亮,周东丰,苏晶.电针对慢性应激抑郁模型大鼠脑单胺类神经递质的影响[J].中华精神科杂志,1999,32(4):220-222. 被引量:174
  • 7Oret C,Lawerenson JG.A comparation of blood-brain barrier and blood-nerve barrier endothelial cell markers[J].Anat Embryol,1999,199:509-517.
  • 8周璇,王雪琦.谷氨酸能和γ氨基丁酸能系统与情感障碍[J].中国神经科学杂志,2003,19(2):130-133. 被引量:21
  • 9Nowak G,Redmond A.Swim stress increases the potency of glycine at the N-methyl-D-aspartate receptor complex[J].Neurochem,1995,64:925-927.

二级参考文献24

  • 1张家俊,陈文为.中药酸枣仁、龙齿、石菖蒲对小鼠脑组织单胺类神经递质及其代谢物的影响[J].北京中医药大学学报,1995,18(6):64-66. 被引量:92
  • 2[1]Steffens DC, Byrum CE, McQuoid DR et al. Hippocampal volume in geriatric depression [J]. Biol Psychiat, 2000, 48:301-309.
  • 3[2]Rajkowska G, Miguel-Hidalgo JJ, Wei J,et al. Morphometric evidence for neuronal and glial prefrontal cell pathology in major depression [J]. Biol Psychiat, 1999, 45: 1085-1098.
  • 4[3]Magistretti P J, Pellerin L, Rothman DL, et al. Energy on demand [J]. Science, 1999, 283: 496-497.
  • 5[4]Mason GF, Haga K, Appel M, et al. Measuring cortical GABA levels and neurotransmitter turnover with 1 H-MRS and 13 C-MRS [J]. Biol Psychiat, 2001,49: 148S.
  • 6[5]Nowak G,Redmond A, McNamara M, et al. Swim Stress increases the potency of glycine at the N-methyl-D-aspartate receptor cornplex[J]. J Neurochem,1995,64: 925-927.
  • 7[6]Fitzgerald LW, Ortiz J, Hamedani AG, et al. Drugs of abuse and stress increase the expression of GluR1 and NMDAR1 glutamate receptor subunits in the rat ventral tegmental area: common adaptations among cross-sensitizing agents [J]. J Neurosci, 1996, 16:274-282.
  • 8[7]Krystal JH, Petrakis IL, D Souza DC, et al. Interactive effects of high dose intravenous glycine and oral D-cycloserine in healthy human subjects [J]. Bid Psychiat, 1997, 41 (Suppl): 23S.
  • 9[8]Bode L, Dietrich DE, Stoyloff R, et al. Amantadine and human Borna disease virus in vitroandin vivoin an infected patients with bipolar depression [J]. Lancet, 1997, 349: 958.
  • 10[9]Berman RM, Cappiello A, Anand A,et al. Antidepressant effects of ketamine in depressed patients [J]. Biol Psychiat, 2000, 47:351-354.

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