期刊
JOURNAL OF STROKE & CEREBROVASCULAR DISEASES
卷 31, 期 4, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.jstrokecerebrovasdis.2022.106352
关键词
Hypoxia-ischemia; White matter injury; Iron stain; Iron content; Lipid peroxidation
资金
- National Natural Science Foundation of China [81501305]
- Fujian Provincial Natural Science Foundation of China [2019J01292]
This study investigated the changes in iron distribution, iron content, and malondialdehyde in different brain regions after hypoxic-ischemic injury in neonatal rats. The results showed that brain iron metabolism changed dynamically in 3-day-old neonatal rats, which may contribute to the pathogenesis of hypoxic-ischemic white matter injury.
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.
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