Administration of secretoneurin is protective in hypoxic–ischemic neonatal brain injury predominantly in the hypoxic-only hemisphere

Highlights • Secretoneurin plasma levels decrease 48 h after experimental hypoxic–ischemic brain injury. • Administration of secretoneurin prior to the decline attenuates brain injury in newborn mice. • Injury mitigation is associated with a reduction in apoptotic cell death predominantly in the hyp...

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Bibliographic Details
Published in:Neuroscience 2017-06, Vol.352, p.88-96
Main Authors: Posod, Anna, Wechselberger, Karina, Stanika, Ruslan Iljitsch, Obermair, Gerald J, Wegleiter, Karina, Huber, Eva, Urbanek, Martina, Kiechl-Kohlendorfer, Ursula, Griesmaier, Elke
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Brain Injuries - etiology
Brain Injuries - prevention & control
Caspase 3 - metabolism
Cell Culture Techniques
Cell Hypoxia - drug effects
Dose-Response Relationship, Drug
Embryo, Mammalian
Functional Laterality - drug effects
Glucose - deficiency
Hippocampus - cytology
Hypoxia-Ischemia, Brain - blood
Hypoxia-Ischemia, Brain - complications
hypoxia–ischemia
hypoxic-only
Mice
Microglia - drug effects
Microglia - pathology
neonatal brain injury
Neurology
Neurons - drug effects
neuropeptide
Neuropeptides - blood
Neuropeptides - pharmacology
Neuropeptides - therapeutic use
neuroprotection
Neuroprotective Agents - blood
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
Proliferating Cell Nuclear Antigen - metabolism
Secretogranin II - blood
Secretogranin II - pharmacology
Secretogranin II - therapeutic use
secretoneurin
Statistics, Nonparametric
Time Factors
Citations: Items that this one cites
Items that cite this one
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Summary:Highlights • Secretoneurin plasma levels decrease 48 h after experimental hypoxic–ischemic brain injury. • Administration of secretoneurin prior to the decline attenuates brain injury in newborn mice. • Injury mitigation is associated with a reduction in apoptotic cell death predominantly in the hypoxic-only hemisphere.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2017.03.055