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中文摘要：
越来越多的证据表明脑内高铁和alpha-突触核蛋白聚集是导致黑质多巴胺（DA）能神经元死亡的关键因素。但是高铁和alpha-突触核蛋白聚集的关系尚未研究清楚。本实验首先在MPTP制备的帕金森病小鼠模型上证实了铁水平和alpha-突触核蛋白的选择性聚集与黑质区和腹侧被盖区DA能神经元的不同易损性之间存在相关性。并在SK-N-SH多巴胺能细胞上证实高表达alpha-突触核蛋白的细胞更易受铁的损伤，而干涉alpha-突触核蛋白后细胞能够抵抗铁对细胞的损伤。高铁导致的alpha-突触核蛋白聚集可通过其mRNA上的铁反应元件（IRE）实现，并且与氧化应激和核转录因子（Nrf2）/血红素加氧酶-1（HO-1）途径的调控异常有关。本研究进一步阐明了铁和alpha-突触核蛋白聚集的相互作用导致DA能神经元损伤的机制。
结论摘要：
英文主题词iron;alpha-synuclein;iron responsive element;heme oxygenase-1;Parkinson's disease
成果综合统计
期刊论文
会议论文
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期刊论文
Curcumin attenuates 6-hydroxydopamine-induced cytotoxicity by anti-oxidation and nuclear factor-kapp
Alpha-synuclein aggregation is involved in the toxicity induced by ferric iron to SK-N-SH neuroblast
Oxidative Stress Partially Contributes to Iron-Induced Alpha-Synuclein Aggregation in SK-N-SH Cells.
会议论文
Up-regulation of divalent metal transporter 1 in 6-hydroxydopamine intoxication is IRE/IRP dependent
Activation of ATP-sensitive potassium channels enhances DMT1-mediated ferrous iron uptake in SK-N-SH
Up-regulation of DMT1+IRE and down-regulation of FP1 are involved in 6-hydroxydopamine-induced neuro
Nifedipine reduces iron accumulation and dopamine neuron degeneration in the iron-overloaded substan
Expression of iron-related proteins and alterations in iron content in the temporal cortex of parkin
Nifedipine reduces iron-overload induced dopamine neuron degeneration by inhibition of iron accumula
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