阿戈美拉汀在Aβ_(25-35)诱导的PC12细胞损伤的保护作用研究  

The protective role of Agomelatine on the Aβ_(25-35) induced damage to PC12 cells

作　　者：姚恺[1] 邬军锋[1] 祖恒兵[1] 

机构地区：[1]复旦大学附属金山医院神经内科,上海201508

出　　处：《神经解剖学杂志》2017年第2期197-201,共5页Chinese Journal of Neuroanatomy

基　　金：上海市金山区卫生和计划生育委员会青年项目(JSKJ-KTQN-2015-05)

摘　　要：目的:研究阿戈美拉汀(Agomelatine)在阿尔茨海默病病理损伤中的保护作用。方法:利用Aβ_(25-35)诱导PC12细胞损伤作为细胞模型,给予Agomelatine预保护,通过Western Blot方法检测Tau蛋白磷酸化的表达情况,流式细胞术检测细胞凋亡率,并检测氧化应激指标MDA水平以及SOD活性。结果:Aβ_(25-35)显著地提高Tau蛋白磷酸化表达以及MDA水平,增加细胞总凋亡率并降低SOD活性(P<0.05),而加入阿戈美拉汀预保护后,与Aβ_(25-35)单独处理组相比,阿戈美拉汀预保护组Tau蛋白磷酸化表达、MDA水平以及细胞总凋亡率明显降低(P<0.05),而SOD活性明显上升(P<0.05)。结论:阿戈美拉汀在Aβ_(25-35)诱导的PC12细胞损伤中具有保护效应。Objective：To study the protective effect of Agomelatine on the pathologic injury of Alzheimer＇s disease.Methods：The Aβ25-35 was added to PC12 cells to set up damage modal.After Agomelatine addition,the expression of p-tau was assessed by Western Blot,the apoptotic rate was assessed by flow cytometry.Then oxidative stress indicators,the level of MDA and the activity of SOD were detected.Results：After Aβ25-35 was added to PC12 cells,the apoptotic rate,the expression of p-tau,the level of MDA were significantly increased,and the SOD activity was remarkablely decreased comparing to control groups （P 〈 0.05）.The pre-treatment of Agomelatine could reduce Aβ25-35 induced the increase of cell apoptosis,MDA level and p-tau expression （P 〈 0.05）.Furthermore,the decrease of SOD activity caused by Aβ25-35 was partly reversed by Agomelatine （P 〈 0.05）.Conclusion：Agomelatine has a protective effect in Aβ25-35 induced damage to PC12 cells.

关 键 词：阿尔茨海默病 阿戈美拉汀 AΒ 氧化应激 细胞凋亡 PC12细胞 AΒ 

分 类 号：R749.16[医药卫生—神经病学与精神病学]