[1]张 泽,韩 锟,贾 宁△.荭草苷对APP/PS1转基因小鼠神经保护作用实验研究*[J].陕西医学杂志,2020,49(5):534-537.
 ZHANG Ze,HAN Kun,JIA Ning..Neuroprotective effect of orientin on APP/PS1 transgenic mice[J].,2020,49(5):534-537.
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荭草苷对APP/PS1转基因小鼠神经保护作用实验研究*
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
49
期数:
2020年5期
页码:
534-537
栏目:
基础研究
出版日期:
2020-05-05

文章信息/Info

Title:
Neuroprotective effect of orientin on APP/PS1 transgenic mice
文章编号:
DOI:10.3969/j.issn.10007377.2020.05.006
作者:
张 泽韩 锟贾 宁
锦州医科大学附属第一医院神经内科(锦州 121001)
Author(s):
ZHANG ZeHAN KunJIA Ning.
Department of Neurology,the First Affiliated Hospital of Jinzhou Medical University(Jinzhou 121001)
关键词:
荭草苷 APP/PS1转基因小鼠 阿尔茨海默病 脑源性神经生长因子 酪氨酸激酶B β-淀粉样蛋白
Keywords:
Orientin APP/PS1 transgenic mice Alzheimer's disease Brain derived neurotrophic factor Tyrosine kinase B β-amyloid protein
分类号:
R745.1
文献标志码:
A
摘要:
目的:探讨荭草苷(Ori)对 APP/PS1转基因小鼠海马神经元的神经保护作用。方法:将10月龄APP/PS1转基因小鼠随机分为模型组(Tg组)、Ori低剂量组(Tg/Ori-L组)和Ori高剂量组(Tg/Ori-H组),将同月龄C57BL/6J小鼠作为对照组(NT组)。采用Morris水迷宫实验检测各组小鼠空间学习、记忆能力; 采用Western blot法检测各组小鼠海马区脑源性神经生长因子(BDNF)、酪氨酸激酶B(TrkB)受体的蛋白表达; 采用ELISA法检测β-淀粉样蛋白1-42(Aβ1-42)水平。结果:与NT组比较,Tg组小鼠寻找平台的逃避潜伏期延长及穿越目的象限的次数减少(P<0.05),海马区BDNF、TrkB受体表达降低(P<0.05),Aβ1-42 表达升高(P<0.05)。与Tg组比较,Tg/Ori-L组和Tg/Ori-H组各指标均显著改善(P<0.05),但Tg/Ori-L组与Tg/Ori-H组间比较无统计学差异(P>0.05)。结论:Ori可以改善APP/PS1小鼠空间学习记忆能力,其机制可能与上调海马神区经元BDNF及TrkB受体表达、减少脑内Aβ沉积有关。
Abstract:
Objective:To explore neuroprotective mechanism of orientin(Ori)on hippocampal neurons of APP/PS1 transgenic mice. Methods:10 months old APP/PS1 transgenic mice were randomly divided into three groups:model group(Tg),Ori low-dose group(Tg/Ori-L)and Ori high-dose group(Tg/Ori-H). C57BL/6J mice of the same age were utilized as control group(NT group). The spatial learning and memory ability of mice in each group were detected by Morris water maze test. The protein expression of BDNF and TrkB receptor in hippocampus of mice in each group were detected by Western blot. The level of Aβ1-42 was detected by ELISA. Results:Compared with NT group,the escape latency of TG group was prolonged and the times of crossing the target quadrant was decreased(P<0.05),the expression of BDNF and TrkB receptor in hippocampus was decreased(P<0.05),and the expression of Aβ1-42 was increased(P<0.05). Compared with TG group,TG/Ori-L group and TG/Ori-H group showed significant improvement(P<0.05),but there was no significant difference between TG/Ori-L group and TG/Ori-H group(P>0.05). Conclusion:Ori can improve the spatial learning and memory ability of APP/PS1 mice,and its mechanism may be related to the up regulation of BDNF and TrkB receptor expression in hippocampal neurons and the reduction of Aβ deposition in brain.

参考文献/References:

[1] Bekinschtein P,Cammarota M,Igaz LM,et al. Persistence of long-term memory storage requires a late protein synthesisand BDNF-dependent phase in the hippocampus[J]. Neuron,2007,53(2):261-277.
[2] Peng S,Wuu J,Mufson EJ,et al. Precursor form of brain-derived neurotrophic factor and mature brain-derived neurotrophic factor are decreased in the pre-clinical stages of Alzheimer's disease[J]. J Neurochem,2005,93(6):1412-1421.
[3] Kemppainen S,Rantamaki T,Jerónimo-Santos A,et al. Impaired TrkB receptor signaling contributes to memory impairment in APP/PS1 mice[J]. Neurobiol Aging,2012,33(6):e23-e39.
[4] 朱 伟,李 志,张 丹.虎杖改善阿尔茨海默病小鼠模型的学习记忆能力及作用机制研究[J].陕西医学杂志,2014,43(12):1574-1581.
[5] Wang S,Yu Y,Feng Y,et al. Protective effect of the orientin on noise-induced cognitive impairments in mice [J]. Behav Brain Res,2016,296:290-300.
[6] Tamminenip P,Jeong YY,Feng T,et al. Impaired axonal retrograde trafficking of the retromer complex augments lysosomal deficits in Alzheimer's disease neurons [J]. Human Molecular Genetics,2017,26(22):4352-66.
[7] Galluzzi L,Baehrecke EH,Ballabio A,et al. Molecular definitions of autophagy and related processes [J]. The EMBO Journal,2017,36(13):1811-36.
[8] Vorhees CV,Williams MT. Morris water maze:procedures for assessing spatial and related forms of learning and memory[J]. Nat Protoc,2006,1(2):848-58.
[9] 刘 涛,张荣超,黄 悦.跑台运动对D-半乳糖致阿尔茨海默病模型大鼠干预的实验研究[J].陕西医学杂志,2014,43(2):149-157.
[10] Marta B,Cinzia G,Fiorenzo C.Peripheral blood brain-derived neurotrophic factor as a biomarker of Alzheimer's disease:Are there methodological biases[J]. Mol Neurobiol,2018,55(8):6661-6672.
[11] Pandya CD,Kutiyanawalla A,Pillai A. BDNF-TrkB signaling and neuroprotection in schizophrenia[J]. Asian J Psychiatr,2013,6(1):22-28.
[12] 郭新荣,王瑞辉,吴 涛,等.不同时机针刺介入对TBI模型大鼠NGF蛋白表达及mRNA水平调控的实验研究[J].陕西中医,2014,35(1):116-118.
[13] Magdalena M,Juan FM,María BZ,et al. Brain-derived neurotrophic factor:a key molecule for memory in the healthy and the pathological brain[J]. Front Cell Neurosci,2019,13:363.
[14] 屈红艳,邢文文,李 璐,等. 针灸调节阿尔茨海默病患者线粒体SIRT3机制初探[J].陕西中医,2014,40(2):244-246.
[15] FrancescoA,Katenina C,Richard P,et al. Amyloid beta soluble forms and plasminogen activation system in Alzheimer's disease:Consequences on extracellular maturation of brain-derived neurotrophic factor and therapeutic implications[J]. CNS Neurosci Ther,2019,25(3):303-313.

备注/Memo

备注/Memo:
*辽宁省自然科学基金指导计划项目(2019-ZD-0616);辽宁省自然科学基金计划项目(2013022028)
更新日期/Last Update: 2020-07-28