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不同剂量多塞平干预对β淀粉样蛋白1-42诱导记忆损伤大鼠的影响 被引量:1

Effects of different doses of doxepin on memory injury in rats induced by β-amyloid142
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摘要 目的研究不同剂量多塞平干预对β淀粉样蛋白(Aβ)1-42诱导记忆损伤大鼠的影响。方法将40只大鼠随机分为正常对照组(A组)、Aβ1-42模型组(B组)、多塞平(1mg/kg)干预组(C组)和多塞平(5mg/kg)干预组(D组),每组各10只,采用侧脑室注射Aβ1-42方法建立Aβ1-42损伤大鼠模型,经多塞平腹腔注射21天后,采用Morris水迷宫检测大鼠的学习记忆能力并进行比较分析。结果与A组相比,B、C、D组大鼠的平台搜索潜伏期明显延长(P〈0.05),平台搜索轨迹评分明显下降(P〈0.05);予多塞平腹腔注射后,与B组相比,C组大鼠的平台搜索潜伏期明显下降(P〈0.05),平台搜索轨迹明显改善(P〈0.05),而D组变化不明显。结论小剂量多塞平对Aβ1-42诱导的大鼠记忆损伤有改善作用。 Objective To investigate the effects of different doses of doxepin on memory injury in rats induced by β-amyloid (Aβ)1-42- Methods Forty rats were randomly divided into control group ( group A ), model group ( group B ), doxepin treatment ( 1 mg/kg ) group ( group C ) and doxepin (5 mg/kg) treatment group(group D),with 10 rats in each group. Aβ1-42 injection into lateral ventricle was used to establish rat memory injury model. Doxepin was administered intraperitoneally for 21 days. Then Morris water maze test was used for evaluation of learning and memory. Results Compared with group A, the rats' platform search latency prolonged obviously (P 〈 0. 05 ) and the platform search trajectory score obviously decreased( P 〈 0. 05 ) in group B and group C, group D. After doxepin injection, compared with group B, the rats' platform search latency decreased obviously( P 〈 0.05 ) and the platform search trajectory obviously improved ( P 〈 0. 05 ) in group C. However, there wasn' t any significant difference in group D compared to group B. Conclusion Doxepin in low dose can improve memory injury in rats induced by A1-1.42.
作者 卜吉梅 祖衡兵 Bu Jimei Zu Hengbing.(Department of Neurology ,Jinshan Hospital ,Fudan University,Shanghai 201508, China)
出处 《临床内科杂志》 CAS 2016年第12期846-848,共3页 Journal of Clinical Internal Medicine
基金 上海市金山区卫计委立项资助项目(JSKJ-KTMS-2014-05)
关键词 多塞平 记忆 β淀粉样蛋白1-42 Doxepin Memory β-amyloid1-42
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  • 1Reddy.PH Abnormal tau,mitochondrial dysfunction,impaired axonal transport of mitochondria,and synaptic deprivation in Alzheimer's disease[J].Brain Res,2011,1415(30):136-148.
  • 2Reddy PH,Beal MF.Amyloid beta,mitochondrial dysfunction and synaptic damage:implications for cognitive decline in aging and Alzheimer's disease[J].Trends Mol Med,2008,14 (2):45-53.
  • 3Lu P,Mamiya T,Lu L,et al.Silibinin attenuates amyloid {beta}2535 peptide-induced memory impairments:implication of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-{alpha}) in mice[J].J Pharmacol Exp Ther,2009,331 (7):319-326.
  • 4Nagakura A,Shitaka Y,Yarimizu J,et al.Characterization of cognitive deficits in a transgenic mouse model of Alzheimer' s disease and effects of donepezil and memantine[J].Euro J Pharmacol,2013,703(1-3):53-61.
  • 5Win-Shwe TT,Fujimaki H,Fujitani Y,et al.Novel object recognition ability in female mice following exposure to nanoparticle-rich diesel exhaust[J].Toxicol Appl Pharmacol,2012,262 (3):355-362.
  • 6Griffin WST,Sheng JG,Roberts GW,et al.Interleukin-1 expression in different plaque types in Alzheimer' s disease:significance in plaque evolution[J].J Neuropathol Exp Neurol,1995,54 (2):276-281.
  • 7Bauer J,Strauss S,Schreiter-Gasser U,et al.Interleukin-6 and α-2macroglobulin indicate an acute-phase state in Alzheimers disease cortices[J].FEBS Lett,1991,285(1):111-114.
  • 8Luzina IG,Keegan AD,Heller NM,et al.Regulation of inflammation by interleukin-4:a review of alternatives[J].J Leukocyte Biol,2012,92(4):753-764.
  • 9Gadani SP,Cronk JC,Norris GT,et al.IL-4 in the brain:a cytokine toremember[J].J Immunol,2012,189 (9):4213-4219.
  • 10Reale M,Iarlori C,Feliciani C,et al.Peripheral chemokine receptors,their ligands,cytokines and Alzheimer's disease[J].J Alzheimer's Dis,2008 14(2):147-159.

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