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

发布时间：2019-04-04 10:22

【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(P0.05),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(P0.05),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。
[Abstract]:Aim to investigate the protective effects of escitalopram (escitalopram,ESC) on hippocampal neurons of Alzheimer's disease induced by 尾-amyloid peptide fragment (尾-amyloid peptide,A 尾 25 / 35), and to explore its possible mechanism. Methods Alzheimer's disease (alzheimer disease,AD) model was induced by A尾 25-35 in hippocampal neurons of rats. They were randomly divided into blank control group, A 尾 group and different ESC groups (0.5, 1.0, 1.5 渭 mol 路L-1). Group A 尾 with different ESC (0.5, 1.0, 1.5 渭 mol 路L-1). The morphology of neurons transfected with adenovirus (adenoviruses-enhanced green fluorescent protein,Ad-EGFP) was observed by fluorescence microscope, and the expression of brain-derived neurotrophic factor (brain derived neurotrophic factor,BDNF (brain derived neurotrophic factor,BDNF) was detected by MTS assay. Results compared with the blank group, the branch and length of neuron in A 尾 group and A 尾 group with different concentration of escitalopram were decreased, and the cell viability was decreased (P0.05). The release of), BDNF was significantly decreased in A 尾 group and A 尾 group (P 0.05). Compared with A 尾 group, the number and length of neuron branches and cell viability in A 尾 group with different ESC increased significantly (P0.05), BDNF release was significantly higher than that in A 尾 group). Conclusion Iscitalopram can significantly improve the survival rate of neurons in Alzheimer's disease model and play a cytoprotective role. The mechanism may be to up-regulate BDNF, and slow down the degeneration of neurons in order to promote the repair of neurons.
【作者单位】：郑州大学第一附属医院神经内一科;河南省高等学校临床医学重点学科开放实验室;
【分类号】：R965

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