DHA Reduces Oxidative Stress after Perinatal Asphyxia: A Study in Newborn Piglets
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Updated: Mar 8, 2026

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
Rønnaug Solberg1, Mariangela Longini, Fabrizio Proietti
1Department of Pediatric Research, University of Oslo, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Insights
Docosahexaenoic acid (DHA) administration after hypoxia-ischemia in newborn piglets reduced oxidative stress in the brain. This suggests DHA may protect against brain injury following perinatal hypoxic-ischemic events.
Area of Science:
- Neuroscience
- Biochemistry
- Pediatrics
Background:
- Perinatal hypoxic-ischemic brain damage is a leading cause of infant mortality and neurological disability.
- Oxidative stress from free radical formation is implicated in this damage.
- Docosahexaenoic acid (DHA), a key brain phospholipid, may offer neuroprotection.
Purpose of the Study:
- To test if DHA protects against lipoperoxidation in the brain after hypoxia-reoxygenation.
- To investigate DHA's neuroprotective effects in a neonatal piglet model.
Main Methods:
- Newborn piglets underwent severe global hypoxia and resuscitation.
- One group received DHA 4 hours post-hypoxia; a control group did not.
- Brain tissue (cortex, hippocampus) was analyzed for lipid peroxidation biomarkers using liquid chromatography-mass spectrometry.
Main Results:
- Biomarkers of lipid peroxidation were significantly lower in the DHA-treated group.
- This reduction was observed in both the cerebral cortex and hippocampus.
- DHA administration demonstrated an antioxidative effect in the brain.
Conclusions:
- DHA administration post-hypoxia shows an antioxidative effect in the neonatal piglet brain.
- These findings suggest DHA has potential as a neuroprotectant after brain injury.
- Further research into DHA's therapeutic role in hypoxic-ischemic events is warranted.
Background:
Perinatal hypoxic-ischemic brain damage is a major cause of acute mortality and chronic neurological morbidity in infants and children. Oxidative stress due to free radical formation and the initiation of abnormal oxidative reactions appears to play a key role. Docosahexanoic acid (DHA), a main component of brain membrane phospholipids, may act as a neuroprotectant after hypoxia-ischemia by regulating multiple molecular pathways and gene expression.
Objectives:
The aims of this study were to test the hypothesis that DHA provides significant protection against lipoperoxidation damage in the cerebral cortex and hippocampus in a neonatal piglet model of severe hypoxia-reoxygenation.
Methods:
Newborn piglets, Noroc (LYLD), were subjected to severe global hypoxia. One group was resuscitated with ambient air (21% group, n = 11) and another also received 5 mg/kg of DHA 4 h after the end of hypoxia (21% DHA group, n = 10). After 9.5 h, tissues from the prefrontal cortex and hippocampus were sampled and the levels of isoprostanes, neuroprostanes, neurofurans, and F2-dihomo-isoprostanes were determined by the liquid chromatography triple quadrupole mass spectrometry technique.
Results:
Lipid peroxidation biomarkers were significantly lower in both the cortex and hippocampus in the DHA-treated group compared with the untreated group.
Conclusions:
The present study demonstrates that DHA administration after severe hypoxia in newborn piglets has an antioxidative effect in the brain, suggesting a protective potential of DHA if given after injuries to the brain.

