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

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 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.

scholarly journals Osteopontin Reduced Hypoxia–Ischemia Neonatal Brain Injury by Suppression of Apoptosis in a Rat Pup Model

Stroke ◽  
2011 ◽  
Vol 42 (3) ◽  
pp. 764-769 ◽  
Author(s):  
Wanqiu Chen ◽  
Qingyi Ma ◽  
Hidenori Suzuki ◽  
Richard Hartman ◽  
Jiping Tang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neonatal Brain ◽  
Neonatal Brain Injury ◽  
Hypoxia Ischemia ◽  
Rat Pup

Vitexin reduces hypoxia–ischemia neonatal brain injury by the inhibition of HIF-1alpha in a rat pup model

2015 ◽  
Vol 99 ◽  
pp. 38-50 ◽  
Author(s):  
Jia-Wei Min ◽  
Jiang-Jian Hu ◽  
Miao He ◽  
Russell M. Sanchez ◽  
Wen-Xian Huang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neonatal Brain ◽  
Neonatal Brain Injury ◽  
Hypoxia Ischemia ◽  
Rat Pup

scholarly journals N-Acetyl Cysteine Restores Sirtuin-6 and Decreases HMGB1 Release Following Lipopolysaccharide-Sensitized Hypoxic-Ischemic Brain Injury in Neonatal Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Gagandeep Singh-Mallah ◽  
Takuya Kawamura ◽  
Maryam Ardalan ◽  
Tetyana Chumak ◽  
Pernilla Svedin ◽  
...  
Keyword(s):  
Brain Injury ◽  
Histone Deacetylases ◽  
High Mobility ◽  
Thiol Oxidation ◽  
Neonatal Brain ◽  
Perinatal Brain Injury ◽  
Neonatal Brain Injury ◽  
Protein Levels ◽  
Hypoxia Ischemia ◽  
Acetyl Cysteine

Inflammation and neonatal hypoxia-ischemia (HI) are important etiological factors of perinatal brain injury. However, underlying mechanisms remain unclear. Sirtuins are a family of nicotinamide adenine dinucleotide (NAD)+-dependent histone deacetylases. Sirtuin-6 is thought to regulate inflammatory and oxidative pathways, such as the extracellular release of the alarmin high mobility group box-1 (HMGB1). The expression and role of sirtuin-6 in neonatal brain injury are unknown. In a well-established model of neonatal brain injury, which encompasses inflammation (lipopolysaccharide, LPS) and hypoxia-ischemia (LPS+HI), we investigated the protein expression of sirtuin-6 and HMGB1, as well as thiol oxidation. Furthermore, we assessed the effect of the antioxidant N-acetyl cysteine (NAC) on sirtuin-6 expression, nuclear to cytoplasmic translocation, and release of HMGB1 in the brain and blood thiol oxidation after LPS+HI. We demonstrate reduced expression of sirtuin-6 and increased release of HMGB1 in injured hippocampus after LPS+HI. NAC treatment restored sirtuin-6 protein levels, which was associated with reduced extracellular HMGB1 release and reduced thiol oxidation in the blood. The study suggests that early reduction in sirtuin-6 is associated with HMGB1 release, which may contribute to neonatal brain injury, and that antioxidant treatment is beneficial for the alleviation of these injurious mechanisms.

scholarly journals Necrostatin Decreases Oxidative Damage, Inflammation, and Injury after Neonatal HI

2010 ◽  
Vol 31 (1) ◽  
pp. 178-189 ◽  
Author(s):  
Frances J Northington ◽  
Raul Chavez-Valdez ◽  
Ernest M Graham ◽  
Sheila Razdan ◽  
Estelle B Gauda ◽  
...  
Keyword(s):  
Cell Death ◽  
Brain Injury ◽  
Oxidative Damage ◽  
Apoptotic Cell ◽  
Death Domain ◽  
Neonatal Brain ◽  
Neonatal Brain Injury ◽  
Markers Of Inflammation ◽  
Gene And Protein Expression ◽  
Hypoxia Ischemia

Necrostatin-1 inhibits receptor-interacting protein (RIP)-1 kinase and programmed necrosis and is neuroprotective in adult rodent models. Owing to the prominence of necrosis and continuum cell death in neonatal hypoxia–ischemia (HI), we tested whether necrostatin was neuroprotective in the developing brain. Postnatal day (P)7 mice were exposed to HI and injected intracerebroventricularly with 0.1 μL of 80 μmol necrostatin, Nec-1, 5-(1H-Indol-3-ylmethyl)-(2-thio-3-methyl) hydantoin, or vehicle. Necrostatin significantly decreased injury in the forebrain and thalamus at P11 and P28. There was specific neuroprotection in necrostatin-treated males. Necrostatin treatment decreased necrotic cell death and increased apoptotic cell death. Hypoxia–ischemia enforced RIP1–RIP3 complex formation and inhibited RIP3–FADD (Fas-associated protein with death domain) interaction, and these effects were blocked by necrostatin. Necrostatin also decreased HI-induced oxidative damage to proteins and attenuated markers of inflammation coincidental with decreased nuclear factor-κB and caspase 1 activation, and FLIP ((Fas-associated death-domain-like IL-1β-converting enzyme)-inhibitory protein) gene and protein expression. In this model of severe neonatal brain injury, we find that cellular necrosis can be managed therapeutically by a single dose of necrostatin, administered after HI, possibly by interrupting RIP1–RIP3-driven oxidative injury and inflammation. The effects of necrostatin treatment after HI reflect the importance of necrosis in the delayed phases of neonatal brain injury and represent a new direction for therapy of neonatal HI.

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