scholarly journals Correction: Ten et al., Complement Component C1q Mediates Mitochondria-Driven Oxidative Stress in Neonatal Hypoxic-Ischemic Brain Injury

2013 ◽  
Vol 34 (1) ◽  
pp. 339-339 ◽  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Complement Component ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

scholarly journals Complement Component C1q Mediates Mitochondria-Driven Oxidative Stress in Neonatal Hypoxic-Ischemic Brain Injury

2010 ◽  
Vol 30 (6) ◽  
pp. 2077-2087 ◽  
Author(s):  
V. S. Ten ◽  
J. Yao ◽  
V. Ratner ◽  
S. Sosunov ◽  
D. A. Fraser ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Complement Component ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

scholarly journals The role of oxidative stress in perinatal hypoxic-ischemic brain injury

2012 ◽  
Vol 140 (1-2) ◽  
pp. 35-41 ◽  
Author(s):  
Brankica Vasiljevic ◽  
Svjetlana Maglajlic-Djukic ◽  
Miroslava Gojnic ◽  
Sanja Stankovic
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Brain Damage ◽  
Ischemic Brain Injury ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
Gpx Activity ◽  
Neurodevelopment Outcome

Introduction. The pathogenesis of perinatal hypoxic-ischemic brain damage is highly complex. Objective. The aim of this study was to assess the role of oxidative stress in hypoxic-ischemic brain injury and subsequent abnormal neurological outcome in infants with perinatal hypoxic-ischemic encephalopathy (HIE). We estimated perinatal oxidative brain damage measuring activity of glutathione peroxidase (GPX) in cerebrospinal fluid (CSF) as an indirect biomarker of free radical production during cerebral hypoxia-ischemia in correlation with the level of intracellular enzyme neuron specific enolase (NSE) in CSF as a biomarker of extend of brain injury. Methods. Ninety neonates (>32 GA) with perinatal HIE were enrolled prospectively. HIE was categorized into three stages according Sarnat and Sarnat clinical scoring system and changes seen on amplitude integrated EEG. CSF for GPX analysis and NSE analysis was taken in the first 72 hours of life. Neurodevelopment outcome was assessed at 12 months of corrected gestational age. Results. GPX activity in CSF was in good relation with clinical stage of HIE (p<0.0001) and GA (p<0.0001) and significantly corresponded with subsequent neurodevelopment outcome (p<0.001). GPX activity in CSF showed a strong correlation with NSE levels in CSF (p<0.001) as the biomarker of extent of brain injury. Conclusion. Our results suggest that oxidative stress might be important contributing factor in perinatal hypoxic-ischemic brain damage, particularly in preterm neonates.

scholarly journals Resveratrol mitigates the oxidative stress mediated by hypoxic-ischemic brain injury in neonatal rats via Nrf2/HO-1 pathway

2018 ◽  
Vol 56 (1) ◽  
pp. 440-449 ◽  
Author(s):  
Yan Gao ◽  
Rongrong Fu ◽  
Jue Wang ◽  
Xue Yang ◽  
Lulu Wen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Neonatal Rats ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

Effect of humic acid on oxidative stress and neuroprotection in hypoxic-ischemic brain injury: part 1

2020 ◽  
pp. 1-10
Author(s):  
Senem Alkan Ozdemir ◽  
Nail Ozdemir ◽  
Ozgur Aksan ◽  
Burak Kınalı ◽  
Gökçen Bilici Güler ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Humic Acid ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

Whole Body Hypothermia and Oxidative Stress in Babies With Hypoxic-Ischemic Brain Injury

2010 ◽  
Vol 43 (4) ◽  
pp. 236-240 ◽  
Author(s):  
Serafina Perrone ◽  
Miklós Szabó ◽  
Carlo Valerio Bellieni ◽  
Mariangela Longini ◽  
Márta Bangó ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Whole Body ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
And Oxidative Stress

Abstract MP15: Hypoxia and Endothelin-1 in Microglial Cell Activation

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Francisco J Rodriguez-Matos ◽  
Sebastian O Castaño-Pesante ◽  
Jose R Romero ◽  
Yaritza Inostroza-Nieves
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Brain Injury ◽  
Cell Activation ◽  
Microglial Cell ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Endothelin 1 ◽  
Tnf Α ◽  
Hypoxic Ischemic Brain Injury

Oxidative stress and inflammatory responses play critical roles in hypoxic-ischemic brain injury. Microglial cells are rapidly activated in response to injury and stressful stimuli, including hypoxia. Endothelin-1 (ET-1) is a potent vasoconstrictor that has been associated with cerebrovascular diseases. Hypoxia stimulates endothelial ET-1 production. However, the role of ET-1 in microglia under hypoxia is not clear. The aim of this project was to characterize the effect of hypoxia in a human microglial cell line, HMC3. We induced hypoxia using a chamber (1% O2, 5% CO2, and 92 % N2) at 37 °C for 4h, 24h, and 48h. MUSE Oxidative Stress Assay was performed to measure reactive oxygen species (ROS) formation, ELISA to determine TNF, IL-6, and ET-1 levels, qPCR to measure gene expression of ET-1, and immunofluorescence staining to visualize and compare the presence of ET-1 in hypoxic and control group cells. It was observed that, when compared to normoxic HMC3 cells, hypoxic HMC3 exposure significantly increased the ROS by a factor of 2.5 (p<0.001, n=3), the pro-inflammatory cytokine TNF-α increased 3.8 times (p<0.01, n=4), and IL-6 increased by a factor of 1.6 (p<0.01, n=4). In addition, hypoxia stimulates ET-1 gene expression 5.0-fold (p<0.001, n=4) and increased protein production 1.3 times (p<0.01, n=4). Consequently, treatment with ET-1 increased the amount of ROS, TNF-α, and IL-6 in HMC3 cells by a factor of 1.4 (p<0.05, n=4), 1.6 (p<0.001, n=4), and 1.9 (p<0.05, n=4), respectively. All these events were blocked by ET-1 receptor A (ETRA) antagonist, BQ123. Our results suggest that hypoxic conditions create a cycle of microglial cell activation leading to increased ROS and ET-1 production that further stimulate microglial cells. Thus, we posit that the ET-1 receptor blockade represents a promising therapeutic approach to regulate microglial cell responses in hypoxic-ischemic brain injury.

scholarly journals Features of pathogenesis and early diagnostic criteria of hypoxic-ischemic brain injury in newborns (part 2)

2021 ◽  
Vol 16 (8) ◽  
pp. 5-14
Author(s):  
V.Yu. Martyniuk ◽  
V.B. Shveikina ◽  
T.K. Znamenska ◽  
L.I. Nikulina
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Brain Injury ◽  
Early Diagnosis ◽  
Intercellular Adhesion ◽  
Developing Brain ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

The article deals with the current problem of neonatology and pediatric neurology — the issues of early diagnosis of perinatal hypoxic-ischemic brain injury in newborns, particularly, in prematurely born children. The work considers modern literature data on the mechanisms of hypoxic-ischemic perinatal brain damage. New data on the functioning, injury, as well as the mechanism of cell death of neuronal and glial origin in the developing brain are presented. It was shown that excitotoxicity (glutamatergic system), oxidative stress and aseptic inflammation are involved in the realization of this mechanism, the final result of which is cell death by necrosis and pathological apoptosis. It was emphasized that in immature neuronal tissue, the death of neurons occurs not only by the above paths, but also due to the combined necrotic-apoptotic (necroptotic) mechanism. The ambiguous role of glutamate receptors in the developing brain is analyzed. Literature data are presented that excitotoxicity, oxidative stress and inflammation against the background of peculiarities mitochondrial functioning in the brain lead to the onset of pathological apoptosis. It has been determined that the most promising in the early diagnosis of hypoxic-ischemic damage to the central nervous system in newborns, in particular premature babies, is the study of the level of neuron-specific proteins and antibodies to them, as well as proteins associated with the plasma membrane — intercellular adhesion molecules. The article analyzes the role of neuronal and glial markers, in particular glial fibrillary acidic protein, ubiquitin C-terminal hydrolase L1, myelin basic protein, as well as the role of pro-inflammatory cytokines in the mechanisms of damage to cells of the developing brain. The role of the membrane protein of cerebral capillary endotheliocytes, an intercellular adhesion molecule 1, as one of the markers of damage to the blood-brain barrier cells in various pathological processes, in particular hypoxia and ischemia, was determined.

Oxidative Stress in Hypoxic-Ischemic Brain Injury

2009 ◽  
pp. 239-254 ◽  
Author(s):  
Laura L. Dugan ◽  
M. Margarita Behrens ◽  
Sameh S. Ali
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

Quercetin alleviates neonatal hypoxic-ischemic brain injury by inhibiting microglia-derived oxidative stress and TLR4-mediated inflammation

2020 ◽  
Vol 69 (12) ◽  
pp. 1201-1213
Author(s):  
Kai Le ◽  
Zhiping Song ◽  
Jie Deng ◽  
Xin Peng ◽  
Jun Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury
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