Lipocalin 2 (Lcn2) has been implicated to play a role in various neurodegenerative diseases, and normalizing its overexpression may be of therapeutic potential. Iron chelators were found to reduce Lcn2 levels in certain animal models of CNS injury. Focusing on Alzheimer's disease (AD), we found that the iron chelators deferoxamine and deferiprone inhibited amyloid-β (Aβ)-induced Lcn2 production in cultured primary astrocytes. Accordingly, Aβ-exposure increased astrocytic ferritin production, indicating the possibility that Aβ induces iron accumulation in astrocytes. This effect was not significantly modulated by Lcn2. Known neuroprotective effects of iron chelators may rely in part on normalization of Lcn2 levels.

中文翻译：

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铁螯合剂抑制了淀粉样β诱导的培养星形胶质细胞中脂质运载蛋白2的产生。

Lipocalin 2（Lcn2）已被暗示在各种神经退行性疾病中起作用，正常化其过表达可能具有治疗潜力。在某些中枢神经系统损伤动物模型中，发现铁螯合剂可降低Lcn2水平。着眼于阿尔茨海默氏病（AD），我们发现铁螯合剂去铁胺和去铁酮抑制了淀粉样β（Aβ）诱导的培养原代星形胶质细胞中Lcn2的产生。因此，Aβ暴露增加星形细胞铁蛋白的产生，表明Aβ诱导星形胶质细胞中铁蓄积的可能性。Lcn2没有明显调节这种作用。铁螯合剂的已知神经保护作用可能部分取决于Lcn2水平的正常化。