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铁代谢与新生儿缺氧缺血性脑损伤

徐开宇, 李凡

中国科学院昆明动物研究所，中国科学院/云南省动物模型与人类疾病机理重点实验室，昆明 650223；昆明医科大学基础医学院病理与病理生理学系，昆明 650500

摘要

铁是神经系统正常发育必不可少的金属元素，受多种因素的调节。近年来的研究表明，铁代谢改变是新生儿缺氧缺血性脑损伤(hypoxic ischemic brain damage, HIBD)重要的发病机制之一，也是造成新生儿HIBD后永久性神经伤残的重要原因。缺氧缺血后机体铁循环发生改变，并随着病程的发展引发脑内铁代谢紊乱，脑内铁蓄积，后经多种途径参与脑内神经细胞的损伤过程。因此，研究缺氧缺血如何造成机体循环铁与脑内铁代谢的改变以及两者间可能存在的联系，阐明铁代谢紊乱在HIBD发生和发展中的机制，将为HIBD的预防和治疗提供依据。本文综述了HIBD发病过程中铁代谢变化及其影响因素，以及铁代谢紊乱如何参与HIBD的发生和发展。

关键词： 铁代谢; 缺氧缺血性脑损伤 ; 铁蓄积

分类号：R363

Iron metabolism and neonatal hypoxic ischemic brain damage

XU Kai-Yu, LI Fan

Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Kunming 650223, China； Department of Pathology and Pathophysiology, School of Basic Medical Sciences, Kunming Medical University, Kunming 650500, China

Abstract

Iron is an essential element for nervous system development, and maintaining a normal iron level in nervous system is controlled by multiple factors. Recent studies reported that iron dysregulation and the following iron metabolic pathways played an important role in hypoxic ischemic brain damage (HIBD) in neonates. Circulatory iron level is altered after hypoxia-ischemia exposure, which may cause abnormal iron deposition in the nervous system followed by neuronal injury. Finding the causing factors for abnormal iron metabolism after hypoxia-ischemia exposure, as well as understanding the mechanisms how iron metabolism contributes to HIBD, will shed lights on HIBD prevention and treatment. In this mini-review, we summarized changes in iron metabolism after neonatal hypoxia-ischemia exposure, its possible regulatory factors and how iron abnormalities contribute to HIBD.

Key words: Iron metabolism; hypoxic ischemic brain damage ; iron accumulation

收稿日期：2016-08-10　　录用日期：2016-10-31

通讯作者：李凡　　E-mail: leefan623@sina.com

引用本文：

徐开宇, 李凡. 铁代谢与新生儿缺氧缺血性脑损伤[J]. 生理学报 2017; 69 (2): 218-224.

XU Kai-Yu, LI Fan. Iron metabolism and neonatal hypoxic ischemic brain damage. Acta Physiol Sin 2017; 69 (2): 218-224