ArticlebioRxiv : the preprint server for biology2025
Temporal and cell-specific changes to cellular iron sequestration and lipid peroxidation in a murine model of neonatal hypoxic-ischemic brain injury.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Iron accumulation and lipid peroxidation are pathophysiologic mechanisms that drive neonatal hypoxic-ischemic (HI) brain injury. Characterization of spatiotemporal changes in these processes will help elucidate their role in ischemic neuronal injury as an initial step towards developing targeted interventions. Methods: HI was induced in post-natal day 9 mice using the modified-Vannucci model. Hippocampal tissue from ipsilateral HI exposed, contralateral hypoxia exposed and sham animals was collected at 6h, 24h, 72h and 7d post-HI. Tissue was subsequently evaluated for markers of cell death (TUNEL), intracellular iron changes (FerroOrange, fluorescent Results: Compared to sham, the HI hippocampus showed increased intracellular labile iron levels that was maximal at 6h post-HI with subsequent elevation in only neuroprostanes at 24h post-HI. TUNEL labeling peaked at 24h post-HI. At 72h, labile iron levels and lipid peroxidation declined corresponding with peak infiltration of ferritin positive microglia/macrophages and the start of TUNEL staining decline. In addition, surviving neurons had increased expression of Gpx4 peaking at 72h post-HI that normalized by 7d post-HI. Conclusions: These findings suggest that following HI, an acute increase in labile iron and DHA peroxidation are correlated with markers of cell death that peak at 24h post-HI. Microglial/macrophage iron sequestration and neuronal antioxidant responses may ameliorate further injury and represent targets for neuroprotective therapies.
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