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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 hippocampal neuronal injury induced by β-amyloid peptide (Aβ25-35) in Alzheimer’s disease and its possible mechanism . Methods Aβ25-35-induced rat model of Alzheimer’s disease (AD) was randomly divided into blank control group, Aβ group, different ESC groups (0.5, 1.0, 1.5μmol·L-1) ), Aβ + different ESC (0.5,1.0,1.5μmol·L-1) group. The morphology of neuronal cells transfected with adenoviruses-enhanced green fluorescent protein (Ad-EGFP) was observed by fluorescence microscopy. The cell viability was detected by MTS assay. The expressions of brain derived neurotrophic factor (BDNF) expression. Results Compared with the blank group, the branch and length of neurons in the Aβ group and the esophadahlipram group with different concentrations of Aβ decreased, the cell viability decreased, the difference was statistically significant (P <0.05), BDNF release decreased; with Aβ group Compared with the control group, the numbers and lengths of neurons in Aβ + ESC group increased and the viability of neurons increased, the difference was statistically significant (P <0.05). BDNF release increased. Conclusion Escitalopram can significantly improve the survival rate of neurons in Alzheimer’s disease model and play a protective role. The mechanism may be through up-regulating BDNF and slowing the degeneration of neurons to promote neuronal repair.