Aniracetam attenuates H202-induced deficiency of neuron Viability，mit0Cnondrla D0tentlal and nlDDOCamDaI 10ng-term potentlanon 0t mlCe ln vitro
文献类型：期刊论文
| 作者 | Wang YF1,2; Li CC1; Cai JX[*]1 |
| 刊名 | neuroscience bulletin
 |
| 出版日期 | 2006 |
| 卷号 | 22期号:5页码:274-280 |
| 关键词 | 双氧水 阿尼西坦 细胞活力 线粒体电位 长时程增强 海马 小鼠 |
| 其他题名 | 阿尼西坦减轻双氧水对小鼠神经元活力、线粒体电位及海马长时程增强的损伤 |
| 通讯作者 | caijx@post.kiz.ac.cn |
| 合作状况 | 其它 |
| 中文摘要 | 目的在脑老化和阿尔茨海默尔氏病人脑中,氧自由基的升高是其神经元发生退行性病变,从而导致突触可塑性和认知障碍的机制之一。本文研究了阿尼西坦(aniracetam,一种治疗老年痴呆的药物)对抗双氧水损伤神经元活力,线粒体电位及海马突触传递长时程增强(Long-term potentiation, LTP)的作用。方法用四甲基偶氮唑盐(3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide,MTT)法测定神经元的活力,用线粒体荧光探针MitoTracker Red (CMX Ros) 研究线粒体电位的变化,用膜片钳方法记录了海马CA1区的突触传递效能。结果200 μmol/L的双氧水明显损伤小鼠大脑皮层原代培养神经元的细胞活力,降低其线粒体电位,而10 μmol/L或100 μmol/L阿尼西坦预处理能明显对抗双氧水对细胞活力和线粒体电位的降低作用。双氧水在不影响基础突触传递的剂量下(20 μmol/L),却能显著抑制海马LTP的诱导。阿尼西坦在100 μmol/L剂量下,对基础突触传递没有明显影响,对正常小鼠脑片CA1区的LTP也没有易化作用,然而,100 μmol/L的阿尼西坦却能显著地恢复由双氧水损伤的海马LTP。结论本研究结果表明,阿尼西坦对双氧水导致的毒性具有较强的神经保护作用,这为临床上用其治疗神经退行性疾病提供了参考依据。 |
| 英文摘要 | Objective It is known that free radicals are involved in neurodegeneration and cognitive dysfunction, as seen in Alzheimer＇s disease （AD） and aging. The present study examines the protective effects of aniracetam against H2O2- induced toxicity to neuron viability, mitochondria potential and hippocampal long-term potentiation （LTP）. Methods Tetrazolium salt 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide （MTT） was used to detect neuronal viability. MitoTracker Red （CMX Ros）, a fluorescent stain for mitochondria, was used to measure mitochondria potential. Electrophysiological technique was carried out to record hippocampual LTE Results H2O2 exposure impaired the viability of neurons, reduced mitochondria potential, and decreased LTP in the CA region of hippocampus. These deficient effects were significantly rescued by pre-treatment with aniracetam （10 ～100μmol/L）. Conclusion These results indicate that aniracetam has a strong neuroprotective effect against H2O2-induced toxicity, which could partly explain the mechanism of its clinical application in neurodegenerative diseases. |
| 收录类别 | 其他 |
| 语种 | 中文 |
| 公开日期 | 2010-08-09 |
| 源URL | [http://159.226.149.42:8088/handle/152453/1101]  |
| 专题 | 昆明动物研究所_发育生物学 昆明动物研究所_其他 |
| 作者单位 | 1.中国科学院昆明动物研究所脑与行为研究室,昆明650223 2.中国科学院研究生院,北京100039 |
| 推荐引用方式 GB/T 7714 | Wang YF,Li CC,Cai JX[*]. Aniracetam attenuates H202-induced deficiency of neuron Viability，mit0Cnondrla D0tentlal and nlDDOCamDaI 10ng-term potentlanon 0t mlCe ln vitro[J]. neuroscience bulletin,2006,22(5):274-280. |
| APA | Wang YF,Li CC,&Cai JX[*].(2006).Aniracetam attenuates H202-induced deficiency of neuron Viability，mit0Cnondrla D0tentlal and nlDDOCamDaI 10ng-term potentlanon 0t mlCe ln vitro.neuroscience bulletin,22(5),274-280. |
| MLA | Wang YF,et al."Aniracetam attenuates H202-induced deficiency of neuron Viability，mit0Cnondrla D0tentlal and nlDDOCamDaI 10ng-term potentlanon 0t mlCe ln vitro".neuroscience bulletin 22.5(2006):274-280. |
入库方式： OAI收割
来源：昆明动物研究所
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