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在小鼠中,阿波利波蛋白E是大脑铁平衡所需的

Juan Ma¹, Qian Guo², Meng-Qi Shen³

¹Department of Neurology, Affiliated Hospital, and Institute of Translational and Precision Medicine, Nantong University, 19 Qi Xiu Road, Nantong, Jiangsu, 226001, China; Laboratory of Neuropharmacology of Pharmacy School, and National Clinical Research Center for Aging and Medicine of Huashan Hospital, Fudan University, Shanghai, 201203, China.

|June 20, 2023

概括

在小鼠中,Apolipoprotein E (ApoE) 缺乏导致大脑铁的增加,破坏铁的平衡. 这种铁的失调有助于通过氧化应激,炎症和铁亡导致神经元损伤.

科学领域:

神经科学是一个神经科学.
生物化学生物化学
遗传学遗传学是一个

背景情况:

众所周知,阿波蛋白E缺乏 (ApoE-/-) 会随着年龄的增长而增加外围组织中的铁积累.
ApoE 缺乏对大脑铁含量和平衡稳定的影响在很大程度上仍未得到研究.

研究的目的:

为了研究Apolipoprotein E (ApoE) 在调节大脑铁平衡中的作用.
为了确定ApoE缺乏对小鼠大脑铁代谢和神经元完整性的影响.

主要方法:

在ApoE-/-小鼠大脑中评估的铁含量,转移素受体1 (TfR1),铁波丁1 (Fpn1),铁调节蛋白 (IRP),氨基酸酶,肝素,粉样蛋白-β 42 (Aβ42),MAP2,活性氧物种 (ROS),细胞因子和谷氨过氧酶4 (Gpx4).
研究了ApoE补充对观察到的表型的影响.

主要成果:

缺少ApoE显著增加了脑铁,TfR1和IRP,同时降低了海马体和基底质中的Fpn1,aconitase和hepcidin.
ApoE缺乏导致Aβ42,MDA,8-异质,IL-1β,IL-6和TNFα的升高,并降低了MAP2和Gpx4.
补充ApoE部分扭转了老年ApoE-/-小鼠的铁相关异常.

结论:

ApoE对于维持大脑铁平衡至关重要.
ApoE 缺乏导致通过增强 TfR1 介导的吸收和减少 Fpn1 介导的出口,大脑积累铁.
由ApoE缺乏引起的神经元损伤主要是由铁过载引起的,导致ROS增加,炎症和铁亡.

关键词:

亚当素和粉样β粉样蛋白.在ApoE KO/ApoE (−/−)) 敲除的Apolipoprotein E小鼠中.大脑的铁代谢铁代谢细胞因子 (cytokines) 是一种细胞因子.谷氨过氧化酶4 (Gpx4) 的作用.国际投资计划 (IRP) 和肝素 (hepcidin) 的使用反应性氧物种 (ROS) 是一种反应性氧物种.在TfR1和Fpn1之间.

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