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.

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 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.

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

Neuroprotection for Premature Birth and Neonatal Brain Injury

2017 ◽  
Author(s):  
Eugene Chang
Keyword(s):  
Preterm Birth ◽  
Brain Injury ◽  
Significant Risk ◽  
Birth Asphyxia ◽  
Significant Risk Factor ◽  
Neonatal Brain ◽  
Perinatal Brain Injury ◽  
Neonatal Brain Injury ◽  
Newborn Brain ◽  
Increased Risk

Preterm birth is associated with increased risk of perinatal brain injury. Although there has been little headway made in reducing preterm birth rates, survival of infants born prematurely has improved greatly. Because of this, the neurodevelopmental consequences related to prematurity have become significant issues, especially in those infants born at less than 32 weeks gestation. Hypoxic-ischemic encephalopathy commonly leads to neonatal brain injury both before and after delivery. While perinatal birth asphyxia accounts for a proportion of neonatal brain injury in neonates younger than 37 weeks, preterm birth is the more significant risk factor. This chapter explores the neurodevelopmental consequences associated with preterm birth, the pathophysiology of perinatal brain injury, and the imaging modalities used to assess the newborn brain. Finally, various neuroprotective interventions in clinical use and in development will be described.

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