摘要
目的:观察奥氮平对瑞典APP基因和早老素1基因双转染N2 a细胞的保护作用。方法:双转染N2 a细胞不同浓度奥氮平及Aβ处理后,应用MTT方法检测细胞活性、BCA法测定细胞的蛋白质含量、酶联免疫吸附法(ELISA)测定双转染N2 a细胞分泌到培养液及细胞内的Aβ水平。结果:奥氮平对Aβ诱导的双转染N2 a细胞的死亡具有保护作用,能够显著降低细胞外Aβ的水平(P<0.05),对细胞内Aβ的水平无影响(P>0.05)。结论:奥氮平能够减少双转染N2 a细胞外Aβ的分泌,推测临床上奥氮平有可能通过此途径保护神经细胞延缓AD发展。
Objective:To investigate olanzapine's protective effect on death of double transfected (Swedish APP gene and presenilinl gene) N2a cells induced by β3-amyloid peptide (Aβ). Methods: Double transfected N2a cells were treated with olanzapine or/and Aβ. The MTT assay was used to determine cell viability, BCA assay to determine the protein content of cells, and the Enzyme-Linked-Immuno-Sorbent Assay (ELISA) to determine the intracellular and extrocellular levels of Aβ produced by double transfected N2a cells. Results:The olanzapine had protective effect on transfected N2a cell death induced by Aβ. The extracellullar Aβ of cells treated with olanzapine decreased significantly comparing to the vehicle ( P 〈 0.05 ) ; the intracellular Aβ did not change significantly (P 〉 0.05). Conclution:This data suggest that olanzapine can decrease the production of β-amyloid peptide 42 in double transfected N2a cells and clinically may be helpful in protecting neuron and slowing down the progression of AD by this means.
出处
《军医进修学院学报》
CAS
北大核心
2006年第2期138-139,共2页
Academic Journal of Pla Postgraduate Medical School