scholarly journals Ischemic Preconditioning Reduces Neurovascular Damage After Hypoxia-Ischemia Via the Cellular Inhibitor of Apoptosis 1 in Neonatal Brain

Stroke ◽  
2013 ◽  
Vol 44 (1) ◽  
pp. 162-169 ◽  
Author(s):  
Wan-Ying Lin ◽  
Ying-Chao Chang ◽  
Chien-Jung Ho ◽  
Chao-Ching Huang
Keyword(s):  
Ischemic Preconditioning ◽  
Inhibitor Of Apoptosis ◽  
Neonatal Brain ◽  
Hypoxia Ischemia ◽  
Neurovascular Damage

Neuroprotection of hypoxic/ischemic preconditioning in neonatal brain with hypoxic-ischemic injury

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Xue Fan ◽  
Huiqing Wang ◽  
Li Zhang ◽  
Jun Tang ◽  
Yi Qu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Ischemic Preconditioning ◽  
Hypoxia Inducible Factor ◽  
Ischemic Injury ◽  
Neonatal Brain ◽  
Protective Mechanisms ◽  
Promote Cell Proliferation ◽  
Vascular Regulation ◽  
Hypoxia Ischemia ◽  
Hypoxic Ischemic Injury

AbstractThe neonatal brain is susceptible to hypoxic-ischemic injury due to its developmental characteristics. Hypoxia-ischemia means a decreased perfusion of oxygen and glucose, which can lead to severe encephalopathy. Although early initiation of therapeutic hypothermia was reported to provide neuroprotection for infants after HI, hypothermia administered alone after the acute insult cannot reverse the severe damage that already has occurred or improve the prognosis of severe hypoxic-ischemic encephalopathy. Therefore, exploring new protective mechanisms for treating hypoxic-ischemic brain damage are imperative. Until now, many studies reported the neuroprotective mechanisms of hypoxic/ischemic preconditioning in protecting the hypoxic-ischemic newborn brains. After hypoxia and ischemia, hypoxia-inducible factor signaling pathway is involved in the transcriptional regulation of many genes and is also play a number of different roles in protecting brains during hypoxic/ischemic preconditioning. Hypoxic/ischemic preconditioning could protect neonatal brain by several mechanisms, including vascular regulation, anti-apoptosis, anti-oxidation, suppression of excitotoxicity, immune regulation, hormone levels regulation, and promote cell proliferation. This review focused on the protective mechanisms underlying hypoxic/ischemic preconditioning for neonatal brain after hypoxia-ischemia and emphasized on the important roles of hypoxia inducible factor 1 signaling pathway.

scholarly journals Nuclear translocation of X-linked inhibitor of apoptosis (XIAP) determines cell fate after hypoxia ischemia in neonatal brain

2008 ◽  
Vol 106 (3) ◽  
pp. 1357-1370 ◽  
Author(s):  
Juliet C. Russell ◽  
Heather Whiting ◽  
Nicholas Szuflita ◽  
Mir Ahamed Hossain
Keyword(s):  
Cell Fate ◽  
Nuclear Translocation ◽  
Inhibitor Of Apoptosis ◽  
Neonatal Brain ◽  
Hypoxia Ischemia

scholarly journals Altered Astrocyte–Neuronal Interactions After Hypoxia-Ischemia in the Neonatal Brain in Female and Male Rats

Stroke ◽  
2014 ◽  
Vol 45 (9) ◽  
pp. 2777-2785 ◽  
Author(s):  
Tora Sund Morken ◽  
Eva Brekke ◽  
Asta Håberg ◽  
Marius Widerøe ◽  
Ann-Mari Brubakk ◽  
...  
Keyword(s):  
Male Rats ◽  
Neonatal Brain ◽  
Neuronal Interactions ◽  
Hypoxia Ischemia

scholarly journals 17β-Estradiol protects the neonatal brain from hypoxia–ischemia

2007 ◽  
Vol 208 (2) ◽  
pp. 269-276 ◽  
Author(s):  
Joseph Nuñez ◽  
Zhengang Yang ◽  
Yuhui Jiang ◽  
Theresa Grandys ◽  
Ilana Mark ◽  
...  
Keyword(s):  
Neonatal Brain ◽  
Hypoxia Ischemia ◽  
17Β Estradiol

scholarly journals Sex-dependent consequences of neonatal brain hypoxia-ischemia in the rat

2016 ◽  
Vol 95 (1-2) ◽  
pp. 409-421 ◽  
Author(s):  
Carlos Alexandre Netto ◽  
Eduardo Sanches ◽  
Felipe Kawa Odorcyk ◽  
Luz Elena Duran-Carabali ◽  
Simone Nardin Weis
Keyword(s):  
Neonatal Brain ◽  
Brain Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Disruption of the Serotonergic System after Neonatal Hypoxia-Ischemia in a Rodent Model

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Kathryn M. Buller ◽  
Julie A. Wixey ◽  
Hanna E. Reinebrant
Keyword(s):  
Clinical Intervention ◽  
Rodent Model ◽  
Neonatal Brain ◽  
Ischemic Brain ◽  
Neonatal Hypoxia ◽  
Brain Injured ◽  
Hypoxia Ischemia ◽  
Stem Damage ◽  
The Brain ◽  
Transporter Expression

Identifying which specific neuronal phenotypes are vulnerable to neonatal hypoxia-ischemia, where in the brain they are damaged, and the mechanisms that produce neuronal losses are critical to determine the anatomical substrates responsible for neurological impairments in hypoxic-ischemic brain-injured neonates. Here we describe our current work investigating how the serotonergic network in the brain is disrupted in a rodent model of preterm hypoxia-ischemia. One week after postnatal day 3 hypoxia-ischemia, losses of serotonergic raphé neurons, reductions in serotonin levels in the brain, and reduced serotonin transporter expression are evident. These changes can be prevented using two anti-inflammatory interventions; the postinsult administration of minocycline or ibuprofen. However, each drug has its own limitations and benefits for use in neonates to stem damage to the serotonergic network after hypoxia-ischemia. By understanding the fundamental mechanisms underpinning hypoxia-ischemia-induced serotonergic damage we will hopefully move closer to developing a successful clinical intervention to treat neonatal brain injury.

scholarly journals Moderate Dietary Restriction Reduces p53-Mediated Neurovascular Damage and Microglia Activation After Hypoxic Ischemia in Neonatal Brain

Stroke ◽  
2012 ◽  
Vol 43 (2) ◽  
pp. 491-498 ◽  
Author(s):  
Yi-Fang Tu ◽  
Pei-Jung Lu ◽  
Chao-Ching Huang ◽  
Chien-Jung Ho ◽  
Ya-Ping Chou
Keyword(s):  
Dietary Restriction ◽  
Microglia Activation ◽  
Neonatal Brain ◽  
Hypoxic Ischemia ◽  
Neurovascular Damage

Lipopolysaccharide and hypoxia/ischemia induced IL-2 expression by microglia in neonatal brain

Neuroreport ◽  
2008 ◽  
Vol 19 (10) ◽  
pp. 997-1002 ◽  
Author(s):  
Sylvie Girard ◽  
Annie Larouche ◽  
Hazim Kadhim ◽  
Marek Rola-Pleszczynski ◽  
Fernand Gobeil ◽  
...  
Keyword(s):  
Neonatal Brain ◽  
Hypoxia Ischemia

scholarly journals Circulating Tight-Junction Proteins Are Potential Biomarkers for Blood-Brain Barrier Function in a Model of Neonatal Hypoxic/Ischemic Brain Injury

2020 ◽  
Author(s):  
Axel Erik Andersson ◽  
Carina Mallard ◽  
Carl Joakim Ek
Keyword(s):  
Brain Injury ◽  
Blood Brain Barrier ◽  
Brain Injuries ◽  
Brain Barrier ◽  
Neonatal Brain ◽  
Ischemic Brain ◽  
Blood Brain ◽  
Hypoxia Ischemia ◽  
The Brain ◽  
Junction Proteins

Abstract BackgroundNeonatal hypoxia-ischemia often leads to lifelong disabilities with limited treatments currently available. The brain vasculature is an important factor in many neonatal brain pathologies but there is a lack of diagnostic tools to evaluate the brain vascular health of neonates in a clinical setting. Measurement of blood-brain barrier tight-junction proteins have shown promise as biomarkers for brain injury in the adult. Here we tested the biomarker potential of tight-junctions in the context of neonatal brain injury.MethodsThe levels of TJ-proteins (occluding, claudin-5, and zonula occludens-1) in both blood plasma and cerebrospinal fluid (CSF) as well as blood-brain barrier function were measured in a clinically relevant hypoxia/ischemia model in neonatal rats.ResultsTemporally acute elevated levels of occludin and claudin-5 could be measured in blood and CSF after hypoxia/ischemia with males generally having higher levels than females. The levels of claudin-5 in CSF correlated with the severity of the brain injury at 24h post- hypoxia/ischemia. Simultaneously, we detected early increase in blood-brain barrier-permeability at 6 and 24h after hypoxia/ischemia.ConclusionsLevels of circulating claudin-5 and occludin are increased after hypoxic/ischemic brain injuries and blood-brain barrier-impairment and have promise as early biomarkers for cerebral vascular health and as a tool for risk assessment of neonatal brain injuries.

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