Brain Ceruloplasmin Expression After Experimental Intracerebral Hemorrhage and Protection Against Iron-Induced Brain Injury.
Brain Ceruloplasmin Expression After Experimental Intracerebral Hemorrhage and Protection Against Iron-Induced Brain Injury.
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DOI：
10.1007/s12975-018-0669-0
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发表时间：
2019-03
影响因子：
6.9
通讯作者：
Xi G
中科院分区：
文献类型：
--
作者：
Liu H;Hua Y;Keep RF;Xi G
血浆铜蓝蛋白（CP）是一种重要的铁氧化酶，通过将有毒的亚铁（Fe 2+）氧化为毒性较小的三价铁（Fe 3+）来维持铁的体内平衡。CP在许多神经退行性疾病中已经得到了很好的研究，但在脑出血（ICH）中还没有深入的研究。本研究旨在探讨脑出血后脑组织CP的表达及CP对Fe ~（2+）所致脑损伤的影响。本研究分为两部分：首先，将自体血注射到大鼠的右侧基底节中，并检测脑中CP表达的时间过程（蛋白质和mRNA）。第二，大鼠右侧基底神经节注射Fe 2+盐水溶液、Fe 2 ++ CP盐水溶液或单独注射盐水。第二部分所有大鼠均进行T2加权磁共振成像和行为学测试，然后取脑进行免疫组织化学和Western印迹。我们发现脑出血后CP在皮质和基底节的神经元和星形胶质细胞上均有表达。时间过程显示，ICH诱导的CP表达从4小时增加到7天，在第3天达到峰值。通过RT-PCR证实脑本身是否能产生CP。外源性CP减少Fe 2+诱导的T2病变，血脑屏障破坏，脑细胞死亡和神经功能缺损。这些结果表明CP在潜在减少ICH诱导的脑损伤中的作用。
Ceruloplasmin (CP) is an essential ferroxidase that is involved in maintaining iron homeostasis by oxidizing toxic ferrous iron (Fe2+) to less-toxic ferric iron (Fe3+). CP has been well studied in many neurodegenerative diseases, but there has not been an in-depth investigation in intracerebral hemorrhage (ICH). This research investigated brain CP expression in rats after ICH and the effect of CP on Fe2+-induced brain injury. This study had two parts: first, rats had injection of autologous blood into the right basal ganglia and the time course of CP expression in brain examined (protein and mRNA). Second, rats had an injection of either Fe2+ in saline, Fe2+ plus CP in saline, or saline alone into the right basal ganglia. All rats in the second part had T2-weighted magnetic resonance imaging and behavioral tests before brains were harvested for immunohistochemistry and Western blotting. We found that CP was expressed on neurons and astrocytes in both cortex and basal ganglia after ICH. The time course showed that ICH induced CP expression increased from 4 hours to 7 days, peaking at day 3. Whether the brain itself can produce CP was confirmed by RT-PCR. Exogenous CP reduced Fe2+-induced T2 lesions, blood-brain barrier disruption, brain cell death and neurological deficits. These results suggest a role of CP in potentially reducing ICH-induced brain injury.
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