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脑区硫胺素缺乏对AD模型小鼠脑神经元线粒体功能的影响

发布时间:2018-01-11 01:05

  本文关键词:脑区硫胺素缺乏对AD模型小鼠脑神经元线粒体功能的影响 出处:《神经解剖学杂志》2015年05期  论文类型:期刊论文


  更多相关文章: 阿尔茨海默病 硫胺素缺乏 线粒体功能障碍 VDAC cytochrome C 小鼠


【摘要】:目的:检测阿尔茨海默病(AD)模型小鼠脑区硫胺素缺乏后,电压依赖性阴离子通道蛋白1(VDAC1)和细胞色素C(cytochrome C)蛋白表达的变化。方法:选用2~3月龄阿尔茨海默病模型小鼠(APP/PS1双转基因小鼠)和野生型(WT)小鼠,根据小鼠脑图谱用立体定位注射法在小鼠右海马齿状回,右前皮质脑区注射维生素B1拮抗剂,导致硫胺素缺乏(TD)。在TD处理后10 d进行动物行为学检测,TD处理后30 d应用免疫荧光、Western Blot及RT-PCR法检测VDAC1和细胞色素C在小鼠注射脑区蛋白的表达和分布并分析线粒体总DNA(mt DNA)的变化。结果:TD处理后APP/PS1小鼠和WT小鼠的主,被动规避行为与对照组相比有显著下降(P0.05),两组小鼠注射脑区的VDAC1和细胞色素C呈现高表达(P0.05),脑组织mt DNA总量增加(P0.05)。结论:硫胺素缺乏可以导致AD模型小鼠和野生型小鼠脑内线粒体功能发生改变。
[Abstract]:Objective: to detect thiamine deficiency in brain region of Alzheimer's disease (AD) mice. Changes in the expression of VDAC1 and cytochrome C in voltage-dependent anion channel protein 1 (VDAC1). Methods: two or three months old mice with Alzheimer's disease (AD) were selected. APP/PS1 double transgenic mice and wild-type WT-mice. According to the mouse brain map, vitamin B1 antagonist was injected into the right hippocampal dentate gyrus and right anterior cortical area of mice by stereotactic injection. The results showed that thiamine was deficient in TD. immunofluorescence was used at 10 days after TD treatment and 30 days after TD treatment. Expression and distribution of VDAC1 and cytochrome C protein in mouse brain were detected by Western Blot and RT-PCR method, and total mitochondrial DNA(mt DNA was analyzed. Results APP/PS1 mice and WT mice were treated with TD-treated APP/PS1 and WT mice. Compared with the control group, the passive circumvention behavior decreased significantly (P 0.05), and the VDAC1 and cytochrome C in the brain area of the two groups showed high expression (P 0.05). Conclusion: thiamine deficiency can result in changes of mitochondrial function in AD model mice and wild-type mice.
【作者单位】: 郑州大学基础医学院人体解剖学教研室;
【基金】:国家自然科学基金(81401015)
【分类号】:R749.16;R-332
【正文快照】: 脑区硫胺素缺乏对AD模型小鼠脑神经元线粒体功能的影响王静,常成,张俊霞,曹静静,方志慧,高晓群*(郑州大学基础医学院人体解剖学教研室,郑州450001)阿尔茨海默病(Alzheimer's disease,AD)是最为常见的神经退行性疾病,其主要病理特点是广泛的神经元与突触丢失,神经原纤维缠结(NF

【共引文献】

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