ArticleJournal of molecular neuroscience : MN2010
Gene network analysis to determine the effects of antioxidant treatment in a rat model of neonatal hypoxic-ischemic encephalopathy.
Article in Journal of molecular neuroscience : MN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Identification and clinical validation of F3 as a peripheral blood biomarker for neonatal hypoxic-ischemic encephalopathy using dataset-specific bioinformatics analysis.Frontiers in pediatrics · 2026Article
- The Proteome of a Healthy Human during Physical Activity under Extreme Conditions.Acta naturae · 2014Article
- Applying systems biology methods to the study of human physiology in extreme environments.Extreme physiology & medicine · 2013Article
- Comprehensive gene expression analysis of cerebral cortices from mature rats after neonatal hypoxic-ischemic brain injury.Journal of molecular neuroscience : MN · 2013Article
- Functional annotation of genes differentially expressed between primary motor and prefrontal association cortices of macaque brain.Neurochemical research · 2013Article
- Hypoxic-ischemic neonatal encephalopathy: animal experiments for neuroprotective therapies.Stroke research and treatment · 2013Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neonatal hypoxic-ischemic (HI) encephalopathy can lead to severe brain damage, and is a common cause of neurological handicaps in adulthood. HI can be resolved by the administration of an antioxidant such as 3-methyl-1-phenyl-2-pyrazolin-5-one (MCI-186). In the present study, we performed comprehensive gene expression and gene network analyses using a DNA microarray to elucidate the molecular events responsible for the selective vulnerability of neurons in neonatal HI brain insult and to examine the underlying mechanisms of the effect of MCI-186 on the pathophysiological events in this condition. We used the modified Levine method (Rice model), which has been widely used as an animal model of this condition. A large difference in gene expression was observed between the Rice model and the control group. Up- and downregulated genes after the HI brain insult were mainly related to immune responses and cell death, and neuronal activity, respectively. The effect of MCI-186 administration on gene expression was much less than and contrary to that of the HI brain insult, reflecting the protective effect of MCI-186 in HI brain insult.
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