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Updated: Aug 16, 2025
Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy
Published on: October 28, 2022
The relationship between miRNA-210 and SCN1B in fetal rats with hypoxic-ischemic brain injury
Hisham Al-Ward1, Ning Liu2, Moussa Omorou2
1Shanghai Institute of Stem Cell Research and Clinical Translation, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200065, China.
Insights
Hypoxic-ischemic brain injury in fetal rats elevates miRNA-210 and HIF-1α while decreasing SCN1B. MiRNA-210 regulates SCN1B expression, contributing to brain injury development.
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- Hypoxic-ischemic (HI) brain injury is a primary cause of neonatal seizures and neurodevelopmental disorders.
- It leads to significant long-term impairments and is a major cause of neonatal mortality.
- Understanding the molecular mechanisms underlying HI brain injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the relationship between microRNA-210 (miRNA-210) and the SCN1B gene in fetal rat brain tissue following hypoxic-ischemic brain injury.
- To elucidate the role of miRNA-210 in the pathogenesis of hypoxic-ischemic encephalopathy (HIE).
Main Methods:
- Establishment of a hypoxic-ischemic animal model in fetal rats.
- Assessment of pathological brain injury after 10 and 30 minutes of hypoxia-ischemia and reperfusion.
- Quantification of expression levels for HIF-1α, HIF-1α mRNA, miRNA-210, and SCN1B in brain tissue.
Main Results:
- Hypoxic-ischemia induced varying degrees of brain damage, including neuronal deformation and cell death, which worsened with longer insult duration.
- Expression of HIF-1α, HIF-1α mRNA, and miRNA-210 was significantly upregulated in HI groups compared to controls, with higher levels in severe injury.
- SCN1B expression was downregulated in both mild and severe HI groups, reaching its lowest point at 30 minutes post-insult.
Conclusions:
- MiRNA-210 is implicated in the development of hypoxic-ischemic encephalopathy (HIE).
- MiRNA-210 appears to regulate SCN1B expression, contributing to the observed pathological changes in the fetal rat brain.
- These findings highlight a potential molecular pathway involved in HI brain injury pathogenesis.
Abstract:
Hypoxic-ischemic brain injury contributes to major neurodevelopmental disorders and is one of the leading causes of seizures, which substantially results in neurodevelopmental impairments with long-lasting outcomes and is one of the main causes of death in neonates. We aimed to investigate the correlation between miRNA-210 and SCN1B, a voltage-gated sodium channel gene, in brain tissue of fetal rats with hypoxic-ischemic brain injury. We found that after 10 min of hypoxia-ischemia, all reperfusion groups showed different degrees of damage. The degree of the injury increased in all the groups after 30 min of hypoxia-ischemia. Those changes include changes in the pericellular lumen, capillaries in the cortex, erythrocytes, enlarged pericellular lumen, the enlarged pericapillary lumen in the cortex, edema around glial cells, enlarged gap to form multiple necrotic foci, deformation of neurons, and loss of cell structure. The expression levels of HIF-1α, miRNA-210, and HIF-1α mRNA were higher in the hypoxic-ischemic groups than that in the control groups, among which the expression levels in the severe group were higher than that in mild group. SCN1B is down-regulated in both the mild and severe groups, and the lowest level was found at 30 min after hypoxia in both groups. MiRNA-210 plays a role in the development of hypoxic-ischemic encephalopathy (HIE) by regulating the expression changes of SCN1B. The brain tissue of fetal rats in the hypoxic-ischemic animal model showed pathological changes of brain injury.
