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Aβ致PC12细胞的损伤机制与多奈哌齐的神经保护作用 被引量:2

Mechanism of PC12 Cells Injury Induced by Aβ and Neuroprotective Effect of Donepezil
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摘要 目的 :研究Aβ2 5 3 5蛋白诱导PC12细胞损伤类型以及多奈哌齐对其的保护作用。方法 :采用细胞培养、MTT、LDH检测、TUNEL和透射电镜技术 ,观察Aβ2 5 3 5蛋白对PC12细胞的损伤类型以及多奈哌齐对其的保护作用。结果 :单纯Aβ 10 μmol·L-1处理细胞后 12h ,即可检测到LDH浓度明显升高 [( 2 85 0± 15 0 )U·L-1] ;2 4h后 ,TUNEL法检测细胞凋亡百分率为 3 2 % ,明显高于多奈哌齐干预组(P <0 0 1) ,细胞增殖活性降低 ;透射电镜观察可见细胞凋亡和变性坏死两种现象并存。给予多奈哌齐保护组细胞 ,凋亡百分率、LDH浓度分别不同程度升高 ,但明显低于单纯Aβ 10 μmol·L-1处理组 (P <0 0 5 ) ;细胞增殖活性也明显高于单纯处理组。结论 :Aβ引起的细胞损伤中凋亡与变性坏死并存。多奈哌齐对Aβ诱导的这两种损伤都有一定的保护作用。 Aim:To study the possible mechanism of cell death induced by soluble Aβ 25-35 and the protective effect of Donepezil on them.Methods:By using cell culture,MTT assays,TUNEL,electron microscope,we measured lactate dehydrogenase(LDH) release rate,cell viability,for observing the effect of Donepezil on Aβ induced apoptosis and necrosis in PC12 cells.Results:MTT assays showed that cell viability decreased under Aβ 25-35 treatment.TUNEL showed that after Aβ treatment the apoptotic cell rate was 32%.Electron microscope showed apoptosis and necrosis occurred.While under Donepezil pretreatement,the apoptotic cell rate was 17% (P<0.01) and LDH release rate decreased compared with the former group.Conclusion:Aβ 25-35 induced PC12 cell apoptosis and necrosis while Donepezil could protect PC12 cells against them both.
出处 《中国临床神经科学》 2004年第2期155-158,共4页 Chinese Journal of Clinical Neurosciences
关键词 损伤机制 多奈哌齐 神经保护作用 细胞凋亡 胆碱酯酶抑制剂 Β淀粉样蛋白 老年性痴呆 cholinesterase inhibitor amyloid beta protein apoptosis
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同被引文献33

  • 1张丽,彭少平,韩蓉,秋建华,顾振纶,秦正红.灵芝酯溶性提取物诱导PC12细胞分化的研究[J].中国药理学通报,2005,21(6):662-667. 被引量:9
  • 2杨伯宁,周三国,谭国鹤,龚健古,蓝玲.学习记忆能力与齿状回神经干细胞增殖的关系研究[J].神经解剖学杂志,2006,22(4):404-408. 被引量:14
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