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（P〈0.05）,两组小鼠注射脑区的VDAC1和细胞色素C呈现高表达（P〈0.05）,脑组织mt DNA总量增加（P〈0.05）。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。
Objective： To detect the expression of voltage-dependent anion channel protein 1 （ VDAC1 ） and cytochrome C protein after the thiamine deficiency（TD） in brain regions of the Alzheimers disease （AD） model mice. Methods：Ac- cording to the mouse brain atlas, we stereotaxically injected the pyrithiamine into the right dentate gyrus and prefrontal cortex brain regions of animals which were 2 to 3-month-old wild type C57BL/6 and Alzheimer＇s disease transgenic mice （App/pss transgenic mice） to establish TD models. Ten days after TD treating, the mice were tested for behaviour. Thir- ty days after TD treating we observed the distribution the expression of VDAC1 and cytochrome C protein and mitochondria DNA within the target brain regions by immunofluorescence, Western Blot and RT-PCR. Results： After TD treating, scores of the active and passive avoidance tests decreased significantly compared with the sham group （ P 〈 0.05 ）, and there is a high expression of the VDAC1 and Cytochrome C protein in the brain regions of both groups of mice （P 〈 0.05 ）. Also, the mtDNA of the brain tissue increased （P 〈 0.05 ）. Conclusion：Thiamine deficiency can lead to the mi- tochondrial function changes in the brain of AD model and wild-type mice.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2015年第5期562-568,共7页
Chinese Journal of Neuroanatomy
基金
国家自然科学基金(81401015)
