To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

Sex differences in neonat… - University of Gothenburg, Sweden Till startsida
Sitemap
To content Read more about how we use cookies on gu.se

Sex differences in neonatal mouse brain injury after hypoxia-ischemia and adaptaquin treatment

Journal article
Authors Kenan Li
Tao Li
Yafeng Wang
Yiran Xu
Shan Zhang
C. Culmsee
Xiaoyang Wang
Changlian Zhu
Published in Journal of Neurochemistry
Volume 150
Issue 6
Pages 759-775
ISSN 0022-3042
Publication year 2019
Published at Institute of Neuroscience and Physiology, Department of Health and Rehabilitation
Institute of Neuroscience and Physiology
Pages 759-775
Language en
Links dx.doi.org/10.1111/jnc.14790
Keywords cell death, hypoxia-inducible factor, neonates, oxidative stress, reactive oxygen species, sex, recombinant-human-erythropoietin, cell-death, oxidative stress, preterm, infants, birth asphyxia, rat model, mitochondria, hypothermia, outcomes, damage, Biochemistry & Molecular Biology, Neurosciences & Neurology
Subject categories Neurosciences

Abstract

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. Hif1 alpha mRNA expression increased after HI, and adaptaquin treatment also stimulated Hif1 alpha mRNA expression, which was also more pronounced in males than in females. However, nuclear translocation of HIF1 alpha protein was decreased after HI, and adaptaquin treatment had no influence on HIF1 alpha expression in the nucleus. These findings demonstrate that adaptaquin treatment is neuroprotective, but the potential mechanisms need further investigation. Open Science Badges This article has received a badge for *Open Materials* because it provided all relevant information to reproduce the study in the manuscript. The complete Open Science Disclosure form for this article can be found at the end of the article. More information about the Open Practices badges can be found at .

Page Manager: Webmaster|Last update: 9/11/2012
Share:

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?