scholarly journals NEONATAL BRAIN INJURY AFTER PERINATAL HYPOXIA/ISCHEMIA AND INTRAUTERINE GROWTH RESTRICTION IN THE PIGLET, DTI, NODDI AND 31P/1H 1H/31P SPECTROSCOPY STUDY

2019 ◽  
Vol 55 (S1) ◽  
pp. 109-109
Keyword(s):  
Brain Injury ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Perinatal Hypoxia ◽  
Spectroscopy Study ◽  
Neonatal Brain ◽  
Neonatal Brain Injury ◽  
Intrauterine Growth ◽  
Hypoxia Ischemia

The brain development of infants with intrauterine growth restriction: role of glucocorticoids

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Ying-xue Ding ◽  
Hong Cui
Keyword(s):  
Endothelial Cells ◽  
Brain Injury ◽  
Intrauterine Growth Restriction ◽  
Growth And Development ◽  
Growth Restriction ◽  
Microvascular Endothelial Cells ◽  
Intrauterine Growth ◽  
Growth Restrictions ◽  
The Brain

Abstract Brain injury is a serious complication of intrauterine growth restriction (IUGR), but the exact mechanism remains unclear. While glucocorticoids (GCs) play an important role in intrauterine growth and development, GCs also have a damaging effect on microvascular endothelial cells. Moreover, intrauterine adverse environments lead to fetal growth restriction and the hypothalamus-pituitary-adrenal (HPA) axis resetting. In addition, chronic stress can cause a decrease in the number and volume of astrocytes in the hippocampus and glial cells play an important role in neuronal differentiation. Therefore, it is speculated that the effect of GCs on cerebral neurovascular units under chronic intrauterine stimulation is an important mechanism leading to brain injury in infants with growth restrictions.

Long non-coding RNA Snhg3 protects against hypoxia/ischemia-induced neonatal brain injury

2020 ◽  
Vol 112 ◽  
pp. 104343 ◽  
Author(s):  
Qing Yang ◽  
Ming-Fu Wu ◽  
Li-Hua Zhu ◽  
Li-Xing Qiao ◽  
Rui-Bin Zhao ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neonatal Brain ◽  
Neonatal Brain Injury ◽  
Non Coding Rna ◽  
Hypoxia Ischemia ◽  
Long Non Coding Rna

GAS5 silencing protects against hypoxia/ischemia-induced neonatal brain injury

2018 ◽  
Vol 497 (1) ◽  
pp. 285-291 ◽  
Author(s):  
Rui-bin Zhao ◽  
Li-hua Zhu ◽  
Jia-Ping Shu ◽  
Li-Xing Qiao ◽  
Zheng-Kun Xia
Keyword(s):  
Brain Injury ◽  
Neonatal Brain ◽  
Neonatal Brain Injury ◽  
Hypoxia Ischemia

scholarly journals Knowledge Gaps and Emerging Research Areas in Intrauterine Growth Restriction-Associated Brain Injury

2019 ◽  
Vol 10 ◽  
Author(s):  
Bobbi Fleiss ◽  
Flora Wong ◽  
Fiona Brownfoot ◽  
Isabelle K. Shearer ◽  
Olivier Baud ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Knowledge Gaps ◽  
Intrauterine Growth ◽  
Research Areas

scholarly journals Resveratrol post-treatment protects against neonatal brain injury after hypoxia-ischemia

Oncotarget ◽  
2016 ◽  
Vol 7 (48) ◽  
pp. 79247-79261 ◽  
Author(s):  
Shulin Pan ◽  
Songlin Li ◽  
Yingying Hu ◽  
Hao Zhang ◽  
Yanlong Liu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Post Treatment ◽  
Neonatal Brain ◽  
Neonatal Brain Injury ◽  
Hypoxia Ischemia

scholarly journals Hypoxic Preconditioning Suppresses Glial Activation and Neuroinflammation in Neonatal Brain Insults

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Chien-Yi Chen ◽  
Wei-Zen Sun ◽  
Kai-Hsiang Kang ◽  
Hung-Chieh Chou ◽  
Po-Nien Tsao ◽  
...  
Keyword(s):  
Brain Injury ◽  
Inflammatory Responses ◽  
Hypoxic Preconditioning ◽  
Glial Activation ◽  
Neonatal Brain ◽  
Mixed Glial Culture ◽  
Neonatal Brain Injury ◽  
Promising Therapeutic Approach ◽  
Hypoxia Ischemia

Perinatal insults and subsequent neuroinflammation are the major mechanisms of neonatal brain injury, but there have been only scarce reports on the associations between hypoxic preconditioning and glial activation. Here we use neonatal hypoxia-ischemia brain injury model in 7-day-old rats andin vitrohypoxia model with primary mixed glial culture and the BV-2 microglial cell line to assess the effects of hypoxia and hypoxic preconditioning on glial activation. Hypoxia-ischemia brain insult induced significant brain weight reduction, profound cell loss, and reactive gliosis in the damaged hemisphere. Hypoxic preconditioning significantly attenuated glial activation and resulted in robust neuroprotection. As early as 2 h after the hypoxia-ischemia insult, proinflammatory gene upregulation was suppressed in the hypoxic preconditioning group.In vitroexperiments showed that exposure to 0.5% oxygen for 4 h induced a glial inflammatory response. Exposure to brief hypoxia (0.5 h) 24 h before the hypoxic insult significantly ameliorated this response. In conclusion, hypoxic preconditioning confers strong neuroprotection, possibly through suppression of glial activation and subsequent inflammatory responses after hypoxia-ischemia insults in neonatal rats. This might therefore be a promising therapeutic approach for rescuing neonatal brain injury.

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