中文摘要：

目的考察蛇床子素（osthole,Ost）对转染APP（595/596）基因的小鼠神经元的保护作用,并探讨其作用机制。方法原代培养小鼠神经元,转染APP（595/596）基因构建AD细胞模型;采用CCK-8法检测神经元存活率;试剂盒法检测乳酸脱氢酶（lactic dehydrogenase,LDH）释放量,评价神经元的损伤程度;TUNEL染色法检测神经元凋亡;免疫荧光化学法检测β-淀粉样蛋白（beta-amyloid peptide,Aβ）和β-分泌酶1（β-site APP cleaving enzyme 1,BACE1）的蛋白表达;RT-PCR检测miRNA-107的表达。结果与模型组比较,Ost干预组神经元的存活率明显升高,LDH释放量明显降低,凋亡率明显降低,Aβ和BACE1的蛋白表达均明显降低,而miRNA-107的表达明显升高。结论 Ost对转染APP（595/596）基因的小鼠神经元具有良好的保护作用,其机制可能与上调miRNA-107表达,抑制BACE1表达,进而减少Aβ生成有关。

英文摘要：

Aim To investigate the neuroprotective effects of osthole（ Ost） on the primary cultured cortical neurons transfected with APP（595/596） gene and its underlying mechanism. Methods Neonatal mouse cortical neurons were transfected with APP（595/596） gene to establish AD cell models for the further study. Then,the cell viability was detected by CCK-8 assay,and the leakage of lactate dehydrogenase（ LDH） was assayed by LDH kit to evaluate the injury degree. Transferasemediated nick end labeling（ TUNEL） was used to evaluate the cell apoptosis. The expression of β-amyloid peptide（ Aβ） and β-site APP cleaving enzyme 1（ BACE1） was measured by immunofluorescence,while the miRNA-107 was measured by RT-PCR. Results Compared to model group,Ost could significantly improve the neurons viability,decrease the LDH release and prevent the apoptosis. Ost also inhibited the expression of Aβ and BACE1 at protein level,while enhanced the expression of miRNA-107 at gene level. Conclusion Ost plays a neuroprotective role in neurons transfected with APP（595/596） gene in part through up-regulating miRNA-107.