Neonatal Brain Hemorrhage: The Role of NonProtein-Bound Iron

S. Perrone, S. Negro, M. Tataranno, A. Santacroce, Carlotta Bracciali, M. Longini, F. Proietti, F. Bazzini, E. Belvisi, G. Buonocore
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引用次数: 1

Abstract

Abstract Intraventricular hemorrhage (IVH) in very preterm infants is a common disease, which can induce long-term consequences. Oxidative stress (OS) occurs easily in preterm newborns due to an imbalance between high free radical (FR) production and the low antioxidant shield, not completely developed at birth. Nonprotein-bound iron (NPBI) concentration in cord blood has been found to be highly predictive for the risk of poor neurodevelopmental outcome. However, at present, no data exist about the exact mechanisms associated with IVH induced by iron-mediated FRs. We propose the hypothesis that hypoxia or ischemia-induced releasing of NPBI is a key regulating event that initiates a vicious circle of excessive FR generation, which in turn participates in edema development, inflammatory reaction, and endothelial injury. This suggests that developing effective neuroprotective strategies for preterm infants requires a detailed understanding of OS reactions and glial responses.
新生儿脑出血:非蛋白结合铁的作用
脑室内出血(IVH)是非常早产婴儿的一种常见疾病,可引起长期后果。由于高自由基(FR)生成和低抗氧化屏障之间的不平衡,早产新生儿容易发生氧化应激(OS)。脐带血中的非蛋白结合铁(NPBI)浓度已被发现对不良神经发育结果的风险具有高度预测性。然而,目前还没有关于铁介导的FR诱导IVH的确切机制的数据。我们提出假设,缺氧或缺血诱导的NPBI释放是一个关键的调节事件,它启动了过量FR生成的恶性循环,进而参与水肿发展、炎症反应和内皮损伤。这表明,为早产儿制定有效的神经保护策略需要详细了解OS反应和神经胶质反应。
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