摘要
目的观察多奈哌齐对β淀粉样蛋白25-35片断(Aβ25-35)诱导原代培养的海马神经元损伤的保护作用及神经元β2烟碱型乙酰胆碱受体(β2-nAChR)的表达。方法在不同时间及采用不同浓度多奈哌齐提前干预培养的海马神经元,之后用Aβ25-35诱导神经元损伤。采用倒置显微镜观察神经元形态学改变,以MTT法测量神经元活性变化,利用免疫荧光法观察不同浓度和不同时间多奈哌齐干预后Aβ25-35损伤神经元β2-nAChR表达情况,并用激光扫描共聚焦显微镜免疫荧光半定量法测量其平均相对荧光强度变化。结果多奈哌齐干预组可减轻Aβ25-35对神经元的损伤。多奈哌齐预处理组神经元β2-nAChR表达明显增加,其平均相对荧光强度明显高于Aβ25-35损伤组。结论多奈哌齐对Aβ25-35诱导损伤神经元的保护作用部分与β2-nAChR的上调有关。
Objective To investigate the neuroprotection of donepezil on β amyloid 25-35 fragment（Aβ25-35）- induced neurotoxicity and the expression of β2 nicotinic acetylcholine receptor （β2-nAChR） in primary cultured hippocampus neurons. Methods The primary cultured hippocampus neurons were pre-treated by different concentrations or different time of donepezil, then the neurons were exposed to Aβ25 -35. The morphological changes of the neurons were observed by inverted microscopy and mono-nuclear cell direct cytotoxicity assay was used to measure the changes of cell viability. The β2-nAChR expression on neurons was demonstrated by immunofluorescence staining. Laser scanning confocal images was used to measure the fluorescence intensity of β2- nAChR in neurons. Results The impairment on neurons were reduced by donepezil. Immunofluorescence staining indicated that the β2-nAChR expression on neurons with pre-treated by donepezil increased significantly and Laser scanning confocal images indicated that the fluorescence intensity of β2-nAChR in the neurons of donepezil groups was higher than Aβ25-35 as group. Conclusions The protective mechanism of donepezil on the neurons induced by Aβ 25-35 might be partialy related with the up-regulation of β2-nAChR.
出处
《中国神经免疫学和神经病学杂志》
CAS
2006年第4期209-212,共4页
Chinese Journal of Neuroimmunology and Neurology
