Pereira C, Agostinho P, Oliveira C R
Center for Neuroscience of Coimbra, Faculty of Medicine, University of Coimbra, Portugal.
Free Radic Res. 2000 Nov;33(5):497-506. doi: 10.1080/10715760000301041.
The cytoprotective effect of vinpocetine [14-ethoxycarbonyl-(3alpha, 16alpha-ethyl)-14,15-eburnamine] was investigated on PC12 cells treated with the amyloid beta-peptides (Abeta) for 24 hours. Vinpocetine was shown to protect cells from the inhibition in redox status induced by exposure to Abeta25-35 and Abeta1-40, the maximal protection being achieved at a vinpocetine concentration of 40 microM. At this concentration, vinpocetine blocked the inhibition of the mitochondrial respiratory chain complexes II-III and IV and completely abolished the depletion of pyruvate levels induced by toxic concentrations of Abeta peptides. Furthermore, the accumulation of ROS in cells exposed to Abeta25-35 and Abeta1-40 evaluated using the fluorescent probe 2',7'-dichlorofluorescin (DCF), was reduced in the presence of 40 microM vinpocetine. Taken together, the data presented herein demonstrate that vinpocetine protects cells from Abeta toxicity, preventing the generation of oxidative stress due to the excessive accumulation of ROS. This study suggests that vinpocetine can exert neuroprotective properties which might be of importance and contribute to its clinical efficacy in the treatment of Alzheimer's disease or other neurodegenerative disorders in which oxidative stress is involved.
研究了长春西汀[14-乙氧羰基-(3α, 16α-乙基)-14,15-长春胺]对用淀粉样β肽（Aβ）处理24小时的PC12细胞的细胞保护作用。结果表明，长春西汀可保护细胞免受暴露于Aβ25-35和Aβ1-40诱导的氧化还原状态抑制，在长春西汀浓度为40μM时可实现最大保护作用。在此浓度下，长春西汀可阻断线粒体呼吸链复合物II-III和IV的抑制，并完全消除毒性浓度的Aβ肽诱导的丙酮酸水平降低。此外，使用荧光探针2',7'-二氯荧光素（DCF）评估，在40μM长春西汀存在下，暴露于Aβ25-35和Aβ1-40的细胞中ROS的积累减少。综上所述，本文提供的数据表明长春西汀可保护细胞免受Aβ毒性，防止因ROS过度积累而产生氧化应激。本研究表明，长春西汀可发挥神经保护作用，这可能具有重要意义，并有助于其在治疗阿尔茨海默病或其他涉及氧化应激的神经退行性疾病中的临床疗效。
