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

Artikel i vetenskaplig tidskrift
Författare Kenan Li
Tao Li
Yafeng Wang
Yiran Xu
Shan Zhang
C. Culmsee
Xiaoyang Wang
Changlian Zhu
Publicerad i Journal of Neurochemistry
ISSN 0022-3042
Publiceringsår 2019
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för hälsa och rehabilitering
Institutionen för neurovetenskap och fysiologi
Språk en
Länkar dx.doi.org/10.1111/jnc.14790
Ämnesord 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
Ämneskategorier Neurovetenskaper

Sammanfattning

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 .

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