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新生大鼠缺氧缺血后脑铁代谢的动态变化

Dynamic Changes in Brain Iron Metabolism in Neonatal Rats after Hypoxia-Ischemia.

作者信息

Hu Ding-Wang, Zhang Geng, Lin Ling, Yu Xuan-Jing, Wang Feng, Lin Qing

机构信息

Laboratory of Clinical Applied Anatomy, Department of Human Anatomy, School of Basic Medical Sciences, Fujian Medical University, No.1 Xuefu North Road, Fuzhou, Fujian 350122, China; Key Laboratory of Brain Aging and Neurodegenerative Diseases of Fujian Province, Fuzhou 350122, China.

Public Technology Service Center, Fujian Medical University, Fuzhou 350122, China.

出版信息

J Stroke Cerebrovasc Dis. 2022 Apr;31(4):106352. doi: 10.1016/j.jstrokecerebrovasdis.2022.106352. Epub 2022 Feb 10.

DOI:10.1016/j.jstrokecerebrovasdis.2022.106352
PMID:35152131
Abstract

OBJECTIVES

The pathogenesis of hypoxic-ischemic white matter injury (WMI) in premature infants is still unclear, and the imbalance of cerebral iron metabolism may play an important role. Our study set out to investigate the changes in iron distribution, iron content and malondialdehyde (MDA) in disparate brain regions (parietal cortex, corpus callosum, hippocampus) within 84 days after hypoxia-ischemia (HI) in neonatal rats and to clarify the role of iron metabolism in WMI.

MATERIALS AND METHODS

We adopted a rat model of hypoxic-ischemic WMI. Alterations in iron metabolism were detected by iron staining and iron assay kits, and the degree of brain injury was determined by MDA assays.

RESULTS

Our results showed that different degrees of brain iron deposition occurred within 28 days after HI, and iron staining was the most obvious 3 days after HI. The iron content increased remarkably at 1-7 d after HI in the mixed tissues, especially at 3 d after HI. While the iron content in the parietal cortex and corpus callosum elevated obviously 14 days after HI. And the change trend of MDA was almost consistent with that of the iron content.

CONCLUSIONS

Our findings revealed that brain iron metabolism changed dynamically in 3-day-old neonatal rats suffering from HI, which may cause lipid peroxidation damage to brain tissues. This process may be one of the pathogeneses of hypoxic-ischemic WMI.

摘要

目的

早产儿缺氧缺血性脑白质损伤(WMI)的发病机制尚不清楚,脑铁代谢失衡可能起重要作用。本研究旨在探讨新生大鼠缺氧缺血(HI)后84天内不同脑区(顶叶皮质、胼胝体、海马)铁分布、铁含量及丙二醛(MDA)的变化,并阐明铁代谢在WMI中的作用。

材料与方法

我们采用缺氧缺血性WMI大鼠模型。通过铁染色和铁检测试剂盒检测铁代谢变化,通过MDA检测确定脑损伤程度。

结果

我们的结果表明,HI后28天内不同程度的脑铁沉积出现,HI后3天铁染色最明显。HI后1-7天混合组织中铁含量显著增加,尤其是HI后3天。而顶叶皮质和胼胝体中铁含量在HI后14天明显升高。MDA的变化趋势与铁含量几乎一致。

结论

我们的研究结果表明,3日龄新生大鼠HI后脑铁代谢动态变化,这可能导致脑组织脂质过氧化损伤。这一过程可能是缺氧缺血性WMI的发病机制之一。

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