艾司西酞普兰对Aβ25-35诱导的大鼠海马神经元损伤的保护作用  

Protective effect of escitalopram on rats hippocampus neurons induced by Aβ 25-35

作　　者：李志红[1,2] 张博爱[1,2] 

机构地区：[1]郑州大学第一附属医院神经内一科,河南郑州450052 [2]河南省高等学校临床医学重点学科开放实验室,河南郑州450052

出　　处：《沈阳药科大学学报》2015年第4期299-303,共5页Journal of Shenyang Pharmaceutical University

摘　　要：目的研究艾司西酞普兰(escitalopram,ESC)对β-淀粉样肽片段(β-amyloid peptide,Aβ25-35)诱导的阿尔茨海默病海马神经元细胞损伤的保护作用,并探讨其可能机制。方法以Aβ25-35诱导大鼠海马神经元细胞建立阿尔茨海默病(alzheimer disease,AD)模型,随机分为空白对照组、Aβ组、不同ESC组(0.5、1.0、1.5μmol·L-1)、Aβ+不同ESC(0.5、1.0、1.5μmol·L-1)组。通过荧光显微镜观察腺病毒(adenoviruses-enhanced green fluorescent protein,Ad-EGFP)转染的神经元细胞形态,MTS法检测细胞活性,Western blot检测脑源性神经营养因子(brain derived neurotrophic factor,BDNF)的表达。结果与空白组比较,Aβ组及Aβ+不同浓度艾司西酞普兰组神经元细胞分支及长度均减少,细胞活力降低,差异有统计学意义(P<0.05),BDNF释放减少;与Aβ组比较,Aβ+不同ESC组神经元细胞分支数目及长度均增加,细胞活力上升,差异有统计学意义(P<0.05),BDNF释放增多。结论艾司西酞普兰能显著改善阿尔茨海默病模型神经元的存活率,发挥细胞保护作用,其机制可能是通过上调BDNF、减缓神经元退行性变以促进神经元的修复。Objective To investigate the protective effect of escitalopram（ESC） on Alzheimer＇s Disease hipp- ocampal neurons induced byfl-amyloid peptide （Aβ25-35）. Methods Primary culture of rat hippocampal neu- rons before AD models were induced by 20 μmol-L- 1 Aβ25-35. The cells were randomly divided into con- trol group, Aft group, ESC （0. 5,1.0,1.5 p, mol. L - 1 ） groups, Aft ＋ ESC （0.5,1.0,1.5 μmol · L - 1） groups. Transfection cells with the expression of green fluorescent protein adenovirus （Ad-EGFP） were examined with morphological observation, MTS assay cellular activity. Expression of brain-derived neurotrophic factor （BDNF） protein was measured by Western blot. Results Compared with the control group ,Aft group, Aβ ＋ different concentrations of ESC groups the lengths of the branches reduced, the cell viability decreased, BD- NF activity decreased. The differences show significance meaning （P 〈 0. 05 ）. Compared with the Aft group, the Aβ ＋ different concentrations of ESC groups number and length of the branches increased, the cell viabil- ity increased, BDNF activity increased, the difference showed significance meaning （P 〈 0. 05 ）. Between the Aft ＋ different concentrations of ESC groups, in the Aβ ＋ 1.5 μmol· L - 1 ESC group, the number and length of neuron branches, the cell viability, BDNF activity were highest. Conclusions Escitalopram can significant- ly improve the AD model cell survival rates, its mechanism may be through the increase of BDNF to prevent the degeneration of neurons and promote restoration of the neurons.

关 键 词：艾司西酞普兰 神经元 腺病毒转染 β-淀粉样肽片段25-35 脑源性神经营养因子 

分 类 号：R743.3[医药卫生—神经病学与精神病学]