文章摘要
张昊 印海翔 徐颺 刘涛生.MK-801 诱导精神分裂症小鼠的c-Fos及NADPH氧化酶通路机制研究[J].,2015,15(22):4252-4256
MK-801 诱导精神分裂症小鼠的c-Fos及NADPH氧化酶通路机制研究
Involvement of c-Fos and NADPH Oxidase Pathway in the Pathogenesis ofSchizophrenia in Mice Induced byMK-801
  
DOI:
中文关键词: 精神分裂症  MK-801  c-Fos  氧化应激
英文关键词: Schizophrenia  MK-801  c-Fos  Oxidative stress
基金项目:国家自然科学基金青年项目(31200844)
作者单位
张昊 印海翔 徐颺 刘涛生 上海梅奥心理健康咨询门诊部 上海市黄浦区精神卫生中心第二军医大学心理与精神卫生学系 
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中文摘要:
      目的:探讨MK-801 诱导的精神分裂症小鼠的相关机制,为相关精神分裂症的临床研究和治疗提供参考。方法:60只昆明小 鼠随机分为3 组:对照组、低剂量模型组和高剂量模型组(n=20)。采用两个剂量NMDA受体拮抗剂MK-801 建立谷氨酸低下精 神分裂症小鼠模型,Western Blot 分析小鼠海马组织中相关蛋白c-Fos 及NADPH 氧化酶亚基(p22、p47、p67)的表达变化。结果: 低剂量MK-801 能够显著增加模型组小鼠的自发活动及刻板行为,且与对照组相比有显著的统计学差异性(P<0.01),c-Fos 蛋白 及NADPH 氧化酶蛋白亚基p22 和p47 的表达均明显高于对照组(P<0.01)。而高剂量的MK-801 对小鼠具有后肢肌力障碍方面 的毒性作用。结论:低剂量的MIK-801 能诱导小鼠精神分裂症模型,且氧化应激及c-Fos的过表达参与了MK-801诱导的小鼠精 神分裂症的发病过程。
英文摘要:
      Objective:To explore the pathogenesis mechanism of schizophrenia induced by MK-801 in order to provide reference for clinical research and treatment.Methods:Mice were divided into 3 groups, control group, low dose group and high dose group (n=20). The schizophrenia mice model was established by injecting MK-801, and the expression of c-Fos and NADPH oxidase units was detected by Western blot.Results:The activity distance and stereotyped behavior were enhanced in the low dose and high dose of MK-801 group (P<0.01), and the expression of c-fos, and the NADPH oxidase units, p22 and p47 were upregulated greatly compared with control group (P<0.01). But high dose of MK-801 indicated toxic role for myodynamia disorder of legs.Conclusion:c-Fos overexpression and oxidative stress participated in the pathogenesis of schizophrenia in mice induced by MK-801.
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