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首页> 外文期刊>European review for medical and pharmacological sciences. >Mitophagy in APPsw/PS1dE9 transgenic mice and APPsw stably expressing in HEK293 cells
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Mitophagy in APPsw/PS1dE9 transgenic mice and APPsw stably expressing in HEK293 cells

机译:APPsw / PS1dE9转基因小鼠的线粒体吞噬和APPsw在HEK293细胞中稳定表达

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OBJECTIVE: To observe mitophagy in APPsw/PS1dE9 transgenic mice and APPsw stably expressing HEK293 cell. MATERIALS AND METHODS: The APPsw /PS1dE9 transgenic mice and 20E2 cell (HEK293 cell with APPsw) was used to be the model of Alzheimer’s disease. We dynamically observed the behavior, mitochondrial structure and mitophagy in brain of APP/PS1 transgenic mice in different age groups. Mitochondrial structure and mitophagy of HEK293 and 20E2 cell in vitro were also recorded. RESULTS: The mitochondrion was changed significantly in APP/PS1 transgenic mice and 20E2 cell. LC3 protein, associated with autophagy, was up-regulated. Mitophagy related protein PINK1 and PARKIN were up-regulated. CONCLUSIONS: Mitophagy disorder may be associated with the pathogenesis of Alzheimer’s Disease through PINK1/Parkin pathway.
机译:目的:观察APPsw / PS1dE9转基因小鼠和稳定表达HEK293细胞的APPsw的吞噬能力。材料与方法:APPsw / PS1dE9转基因小鼠和20E2细胞(带有APPsw的HEK293细胞)被用作阿尔茨海默氏病的模型。我们动态观察了不同年龄组APP / PS1转基因小鼠的行为,线粒体结构和线粒体在大脑中的行为。还记录了HEK293和20E2细胞的线粒体结构和线粒体。结果:APP / PS1转基因小鼠和20E2细胞线粒体发生明显变化。与自噬相关的LC3蛋白被上调。线粒体相关蛋白PINK1和PARKIN上调。结论线粒体疾病可能通过PINK1 / Parkin途径与阿尔茨海默氏病的发病机制有关。

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