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背景:许多研究表明淀粉样β蛋白在阿尔茨海默病的发病中起着主要的作用,淀粉样β蛋白的减少将延缓阿尔茨海默病的发展,因此减少淀粉样β蛋白的产生成为干预阿尔茨海默病的一项重要策略。许多阿尔茨海默病患者因精神行为异常而接受抗精神病药物治疗,非典型抗精神病药物奥氮平与喹硫平能够明显地改善阿尔茨海默病患者临床整体印象评分,早期开始的长期干预能够改善患者预后。目的:观察奥氮平与喹硫平对双转染(瑞典淀粉样β蛋白前体蛋白基因和早老素1基因)鼠成神经瘤细胞分泌淀粉样β蛋白42的作用。设计:以细胞为研究对象,完全随机分组设计,对照实验研究。材料:所有研究工作均在加拿大萨斯卡彻温大学医学院神经精神研究所进行。鼠N2a成神经瘤细胞与双转染N2a细胞由康奈尔大学医学院神经病学及神经科学系提供。干预:双转染N2a细胞分别予200μmol/L奥氮平及50μmol/L喹硫平处理24h后,应用酶联免疫吸附反应法测定细胞内外淀粉样β蛋白的水平。应用四甲基偶氮唑盐方法检测细胞活性、BCA法测定细胞的蛋白质含量、免疫印迹检测N2a与双转染N2a细胞淀粉样β蛋白前体蛋白的表达、酶联免疫吸附法测定双转染N2a细胞分泌到培养液及细胞内的淀粉样β蛋白42水平。主要观察指标:测定双转染N2a细胞分泌到培养液及细胞内的淀?
BACKGROUND: Many studies have shown that amyloid beta protein plays a major role in the pathogenesis of Alzheimer’s disease. Decreased amyloid beta protein will delay the development of Alzheimer’s disease and thus reduce amyloid beta production as an intervention Alzheimer’s disease is an important strategy. Many patients with Alzheimer’s disease are treated with antipsychotics due to abnormal mental behavior. Olanzapine and quetiapine, which are atypical antipsychotics, significantly improve clinical overall impression score in patients with Alzheimer’s disease. Long-term early intervention Can improve patient outcomes. OBJECTIVE: To observe the effect of olanzapine and quetiapine on the secretion of amyloid-beta-protein 42 by double transfection (Swedish Amyloid Precursor Protein Gene and Presenilin 1 Gene) murine neuroblastoma cells. Design: Cell research, completely randomized design, controlled experimental study. Materials: All research was performed at the Neuropsychiatric Institute at Saskatchewan University School of Medicine in Canada. N2a neuroblastoma cells and double transfection N2a cells were provided by the Department of Neurology and Neurosciences at Cornell Medical College. Intervention: Double transfection of N2a cells were treated with 200μmol / L olanzapine and 50μmol / L quetiapine respectively for 24 hours. The levels of amyloid β protein in the cells were measured by enzyme-linked immunosorbent assay (ELISA). Cell viability was measured by MTT method. The protein content of cells was determined by BCA method. The expression of amyloid beta protein precursor protein was detected by Western blotting in N2a cells and N2a cells. Enzyme-linked immunosorbent assay N2a cells secreted into the culture medium and intracellular amyloid-beta protein 42 levels. MAIN OUTCOME MEASURES: To determine whether the double transfection of N2a cells secreted into the culture medium and intracellular sediment