Sex differences in neonatal mouse brain injury after hypoxia-ischemia and adaptaquin treatment.
Animals
Animals, Newborn
Female
Hypoxia-Inducible Factor-Proline Dioxygenases
/ antagonists & inhibitors
Hypoxia-Ischemia, Brain
/ metabolism
Male
Mice
Mice, Inbred C57BL
Neuroprotective Agents
/ pharmacology
Oxidative Stress
/ drug effects
Pyridines
/ pharmacology
Quinolines
/ pharmacology
Sex Characteristics
cell death
hypoxia-inducible factor
neonates
oxidative stress
reactive oxygen species
sex difference
Journal
Journal of neurochemistry
ISSN: 1471-4159
Titre abrégé: J Neurochem
Pays: England
ID NLM: 2985190R
Informations de publication
Date de publication:
09 2019
09 2019
Historique:
received:
09
03
2019
revised:
28
05
2019
revised:
24
04
2019
accepted:
06
06
2019
pubmed:
13
6
2019
medline:
24
3
2020
entrez:
13
6
2019
Statut:
ppublish
Résumé
Hypoxia-inducible factor prolyl 4-hydroxylases (HIF-PHDs) are important targets against oxidative stress. We hypothesized that inhibition HIF-PHD by adaptaquin reduces hypoxic-ischemic brain injury in a neonatal mouse model. The pups were treated intraperitoneally immediately with adaptaquin after hypoxia-ischemia (HI) and then every 24 h for 3 days. Adaptaquin treatment reduced infarction volume by an average of 26.3% at 72 h after HI compared to vehicle alone, and this reduction was more pronounced in males (34.8%) than in females (11.7%). The protection was also more pronounced in the cortex. The subcortical white matter injury as measured by tissue loss volume was reduced by 24.4% in the adaptaquin treatment group, and this reduction was also more pronounced in males (28.4%) than in females (18.9%). Cell death was decreased in the cortex as indicated by Fluoro-Jade labeling, but not in other brain regions with adaptaquin treatment. Furthermore, in the brain injury area, adaptaquin did not alter the number of cells positive for caspase-3 activation or translocation of apoptosis-inducing factor to the nuclei. Adaptaquin treatment increased glutathione peroxidase 4 mRNA expression in the cortex but had no impact on 3-nitrotyrosine, 8-hydroxy-2 deoxyguanosine, or malondialdehyde production. Hif1α mRNA expression increased after HI, and adaptaquin treatment also stimulated Hif1α mRNA expression, which was also more pronounced in males than in females. However, nuclear translocation of HIF1α protein was decreased after HI, and adaptaquin treatment had no influence on HIF1α expression in the nucleus. These findings demonstrate that adaptaquin treatment is neuroprotective, but the potential mechanisms need further investigation. Read the Editorial Highlight for this article on page 645.
Substances chimiques
Neuroprotective Agents
0
Pyridines
0
Quinolines
0
adaptaquin
0
Hypoxia-Inducible Factor-Proline Dioxygenases
EC 1.14.11.29
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
759-775Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2019 International Society for Neurochemistry.
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