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8-氧鸟嘌呤脱氧核苷在快速老化小鼠SAMP8海马中表达的增龄性变化研究 被引量:1

The Age-related Increase of 8-oxo-7,8-dihydroguanine in the Hippocampus of Senescence-accelerated Mice Prone 8
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摘要 目的观察8-氧鸟嘌呤脱氧核苷(8-oxo-7,8-dihydroguanine,8-oxo-dG)在快速老化小鼠SAMP8海马不同区域的表达,探讨其变化与SAMP8增龄的关系。方法选用1、4、8、12月龄快速老化小鼠SAMP8(每组各6只),对照组为同龄抗快速老化小鼠SAMR1(每组各6只),用免疫组化法检测海马不同区域内8-oxo-dG的表达水平。结果8-oxo-dG在海马不同区域均有表达,且主要在海马神经细胞胞核内表达。对照组SAMR1小鼠海马各区域8-oxo-dG的吸光度定量结果显示各月龄组间无统计学差异(P>0.05);1、4月龄组SAMP8小鼠海马各区域8-oxo-dG的吸光度定量结果与同龄匹配的SAMR1小鼠间无统计学差异(P>0.05);8、12月龄组SAMP8小鼠海马各区域8-oxo-dG的吸光度定量结果分别显著高于1月龄和4月龄组(P<0.05),也分别显著高于同龄SAMP1对照组(P<0.05)。结论8-oxo-dG在SAMP8快速老化小鼠海马中的水平随增龄而显著增高。 Objective To investigate the age-related expression of 8-oxo-7,8-dihydroguanine (8-oxo-dG) in the mouse hippocampus of senescence-accelerated mice prone 8(SAMP8). Methods Randomly selected 1-, 4-, 8- and 12-month old SAMP8 and the age-matched control strain accelerated mice resistant 1 (SAMR1), with 6 mice in each group, immunohistochemistry analysis was used to explore the ways of change in the two strains of mice. Results 8-oxo-dG could be detected almost exclusively in the nuclei of neurons throughout the whole hippocampus of both strains at all tested age groups. No significant change was observed in CA1 and CA3 subregions among the four SAMR1 groups. Compared with the age-matched SAMR1 mice, no significant difference in 8-oxo-dG expression was observed in 1- and 4-month SAMP8 mice. However, significant increases of 8-oxo-dG in 8- and 12-month SAMP8 mice were observed, compared with the 1-month SMP8 group and with the age-matched SAMR1 groups. The pattern of change in CA3 was similar with that in CA1. ConeluSiolm 8-oxo-dG in the hippocampus of SAMP8 mice increased markedly with the gaining of age.
出处 《中国神经免疫学和神经病学杂志》 CAS 2009年第6期414-417,共4页 Chinese Journal of Neuroimmunology and Neurology
基金 科技部国际科技合作计划基金资助项目(2006DFB31410)
关键词 8-oxo—dG SAMP8 氧化应激 阿尔茨海默病 8-oxo-dG SAMP8 oxidative stress Alzheimer disease
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  • 1蔡剑平,黑爱莲.快速老化痴呆模型小鼠SAMP8学习记忆能力的增龄性变化[J].中国神经免疫学和神经病学杂志,2005,12(4):219-222. 被引量:15
  • 2Morley JE. The SAMP8 mouse: a model of Alzheimer disease. Biogerontol, 2002, 3: 57-60.
  • 3Mecocci P, MacGarvey U, Beal MF. Oxidative damage to mitochondrial DNA is increased in Alzheimer's disease. AnnNeurol, 1994, 36:747-751.
  • 4Lovell MA, Xie C, Markesbery WR. Decreased base excision repair and increased helicase activity in Alzheimer's disease brain. Brain Res, 2000, 85: 116-123.
  • 5Furuta A, Iida T, Nakabeppu Y, et al. Expression of hMTH1 in the hippocampi of control and Alzheimer's disease. Neuroreport, 2001, 12:2895-2899.
  • 6Cai JP, Ishibashi T, Takagi Y, et al. Mouse MTH2 protein which prevents mutations caused by 8-oxoguanine nucleotides. Biochem Biophys Res Commun, 2003, 305:1073-1077.
  • 7Wang J, Xiong S, Xie C, et al. Increased oxidative damage in nuclear and mitochond rial DNA in Alzheimer's disease. J Neurochemist, 2005, 93:953-962.
  • 8Butterfield DA, Boyd-Kimball D, Castegna A. Proteomics in Alzheimer's disease: insights into potential mechanisms of neurodegeneration. J Neurochem, 2003, 86 : 1313-1327.
  • 9Zhu X, Raina AK, Lee HG, et al. Oxidative stress signalling in Alzheimer's disease. Brain Res, 2004, 1000:32-39.
  • 10Takeda T, Hosokawa M, Takeshita S, et al. A new murine model of accelerated senescence[J]. Mech Aging, 1981,17:183-194.

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  • 1Olanow CW, Stern MB, Sethi K. The scientific and clinical basis for the treatment of Parkinson disease[J]. Neurology, 2009, 72(21 Suppl 4): S1-136.
  • 2Noelker C, Hampel H, Dodel R. Blood-based protein biomar kers for diagnosis and classification of neurodegenerative dis eases: current progress and clinical potential [J]. Mol Diagn Ther, 2011, 15:83 102.
  • 3Ahamura S, Muckenthaler MU. Iron toxicity in diseases of aging: Alzheimer's disease, Parkinson's disease and athero sclerosis [J]. Alzheimers Dis, 2009, 16: 879-895.
  • 4Weisskopf MG, O'Reilly E, Chen H, et al. Plasma urate and risk of Parkinson' s disease [J]. Am J Epidemiol, 2007, 166:561-567.
  • 5Yang L, Beal M F . determination of neurotransmitter levels in models of Parkinson' s disease by HPLC-ECD [J]. Methods Mol Boil, 2011, 793:401-415.
  • 6Park HJ, Shin SY, Lee BR, et al. Mesenehymal stem cells augment neurogenesis in the subventricular zone and enhance differentiation of neural precursor ceils into dopaminergic neu rons in the substantia nigra of a Parkinsonian model [J]. Cell Transplant, 2012, 21:1629-1640.
  • 7Meredith GE, Totterdell S, Potashkin JA, et al. Modeling PD pathogenesis in mice: advantages of a chronic MPTP protocol [J]. Parkinsonism Relat Disord, 2008, 14 (Suppl 2) S112-S115.
  • 8O' Malley AJ, Zou KH. Bayesian multivariate hierarchial transformation models for ROC analysis[J]. Stat Med, 2006, 25: 459-479.
  • 9Seer RC, Lee CY, Lira EC, et al. Oxidative damage in Parkinson disease: Measurement using accurate biomarkers[J]. Free Radic Biol Med, 2010,48:560-566.
  • 10Chen-Plotkin AS, Hu WT, Siderowf A, et al. Plasma epidermal growth factor levels predict cognitive decline in Parkinson disease [J]. Ann Neurol, 2011, 69:655-663.

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