scholarly journals α-Tocopherol at Nanomolar Concentration Protects Cortical Neurons against Oxidative Stress

2017 ◽  
Vol 18 (1) ◽  
pp. 216 ◽  
Author(s):  
Irina Zakharova ◽  
Tatiana Sokolova ◽  
Yulia Vlasova ◽  
Liubov Bayunova ◽  
Maria Rychkova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Nanomolar Concentration

Nrf2 mediates the neuroprotective effect of isoflurane preconditioning in cortical neuron injury induced by oxygen-glucose deprivation

2021 ◽  
pp. 096032712198941
Author(s):  
X-S Liu ◽  
X-L Bai ◽  
Z-X Wang ◽  
S-Y Xu ◽  
Y Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neuron ◽  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Lactate Dehydrogenase Activity ◽  
Primary Mouse ◽  
Ldh Release ◽  
Neuron Injury ◽  
And Oxidative Stress

Objective: To investigate how nuclear factor-E2-related factor 2 (Nrf2) involved in the protective effect of isoflurane (Iso) preconditioning in oxygen glucose deprivation (OGD)-induced cortical neuron injury. Methods: Primary mouse cortical neurons were divided into Control, ML385 (an Nrf2 inhibitor), Iso, Iso + ML385, OGD, ML385 + OGD, Iso + OGD, and Iso + ML385 + OGD groups. Lactate dehydrogenase activity (LDH) release and oxidative stress indexes were quantified. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect cell viability, Annexin V-FITC/propidium iodide (PI) staining to measure cell apoptosis, dichloro-dihydro-fluorescein diacetate (DCFH-DA) method to test reactive oxygen species (ROS), and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blotting to evaluate genes and protein expression. Results: Iso preconditioning reduced LDH release and inhibited cell cytotoxicity in OGD-induced cortical neurons, which was abolished by ML385. Iso preconditioning increased the Nrf2 nuclear translocation in cortical neurons. Meanwhile, Iso decreased the OGD-induced apoptosis with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2, which was reversed by ML385. OGD enhanced the level of ROS and malondialdehyde (MDA) in cortical neurons, but reduced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), which were aggravated in ML385 + OGD group and mitigated in Iso + OGD group. No observable difference was found between OGD group and Iso + ML385 + OGD group regarding apoptosis-related proteins and oxidative stress-related indexes. Conclusion: Iso preconditioning up-regulated Nrf2 level to play its protective role in OGD-induced mouse cortical neuron injury.

scholarly journals Neurotherapeutic Effect of Inula britannica var. Chinensis against H2O2-Induced Oxidative Stress and Mitochondrial Dysfunction in Cortical Neurons

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 375
Author(s):  
Jin Young Hong ◽  
Hyunseong Kim ◽  
Junseon Lee ◽  
Wan-Jin Jeon ◽  
Seung Ho Baek ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cortical Neurons ◽  
Inflammatory Diseases ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects ◽  
Neuronal Viability ◽  
Inula Britannica ◽  
Oxidative Effects

Inula britannica var. chinensis (IBC) has been used as a traditional medicinal herb to treat inflammatory diseases. Although its anti-inflammatory and anti-oxidative effects have been reported, whether IBC exerts neuroprotective effects and the related mechanisms in cortical neurons remain unknown. In this study, we investigated the effects of different concentrations of IBC extract (5, 10, and 20 µg/mL) on cortical neurons using a hydrogen peroxide (H2O2)-induced injury model. Our results demonstrate that IBC can effectively enhance neuronal viability under in vitro-modeled reaction oxygen species (ROS)-generating conditions by inhibiting mitochondrial ROS production and increasing adenosine triphosphate level in H2O2-treated neurons. Additionally, we confirmed that neuronal death was attenuated by improving the mitochondrial membrane potential status and regulating the expression of cytochrome c, a protein related to cell death. Furthermore, IBC increased the expression of brain-derived neurotrophic factor and nerve growth factor. Furthermore, IBC inhibited the loss and induced the production of synaptophysin, a major synaptic vesicle protein. This study is the first to demonstrate that IBC exerts its neuroprotective effect by reducing mitochondria-associated oxidative stress and improving mitochondrial dysfunction.

Developmental Expression of Calcium-Binding Protein-Containing Neurons in Neocortical Transplants

1998 ◽  
Vol 7 (2) ◽  
pp. 121-129 ◽  
Author(s):  
Jeffrey M. Rosenstein ◽  
Newton S. More ◽  
Nina Mani ◽  
Janette M. Krum
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Calcium Binding ◽  
Binding Protein ◽  
Substantial Reduction ◽  
Qualitative Change ◽  
Afferent Input ◽  
Calcium Binding Protein ◽  
Developmental Expression ◽  
Parvalbumin Neurons

The present study examined the development of calcium binding protein-containing neurons in a timed series of fetal neocortical transplants. The immunoexpression of parvalbumin and calbindin, which are subpopulations of GABAergic neurons, have been widely studied in normal development and in disease and injury states. Because of their purported resistance to oxidative injury by their ability to buffer Ca++ influx, these neurons have been particularly studied following ischemia. Because it is likely that oxidative stress is associated with the grafting procedure, we sought to determine if these neurons displayed enhanced survival characteristics. Normally, parvalbumin and calbindin represent about 5-10% of cortical neurons. Within 2-4 wk after grafting the expression of both proteins increased markedly in that a relatively larger number of neurons (27% for parvalbumin) were immunopositive. This increase was transitory, however, and by 4 mo and beyond, confocal microscopic data showed a reduction of over 50% of parvalbumin (+) neurons and processes. Calbindin (+) processes showed a qualitative change in that they were smaller with less terminal branching. Electron microscopy confirmed a substantial reduction in parvalbumin synaptic contacts. Interestingly, in older grafts, remaining parvalbumin neurons were those that were strongly NSE (+) suggesting a link between normal metabolism and Ca++ buffering in grafted neurons. It is possible that in early grafts certain neuronal populations transiently upregulated calcium binding proteins as a defensive mechanism against Ca++ influx associated with oxidative stress. Over time, however, following physiological normalization within grafts, the calcium binding protein (+) neurons are diminished, possibly due to lack of appropriate afferent input to the interneuronal pool.

scholarly journals Chronic exposure to U18666A is associated with oxidative stress in cultured murine cortical neurons

2006 ◽  
Vol 98 (4) ◽  
pp. 1278-1289 ◽  
Author(s):  
Chor Hui Vivien Koh ◽  
Matthew Whiteman ◽  
Qiao-Xin Li ◽  
Barry Halliwell ◽  
Andrew M. Jenner ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Chronic Exposure

scholarly journals Nanomolar concentration of triclocarban increases the vulnerability of rat thymocytes to oxidative stress

2013 ◽  
Vol 38 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Yasuhiro Kanbara ◽  
Kazuyoshi Murakane ◽  
Yumiko Nishimura ◽  
Masaya Satoh ◽  
Yasuo Oyama
Keyword(s):  
Oxidative Stress ◽  
Nanomolar Concentration

Low level laser therapy reduces oxidative stress in cortical neurons in vitro

2012 ◽  
Author(s):  
Ying-Ying Huang ◽  
Clark E. Tedford ◽  
Thomas McCarthy ◽  
Michael R. Hamblin
Keyword(s):  
Oxidative Stress ◽  
Laser Therapy ◽  
Cortical Neurons ◽  
Low Level Laser Therapy ◽  
Low Level ◽  
Low Level Laser ◽  
Level Laser

Bromoalkaloids Protect Primary Cortical Neurons from Induced Oxidative Stress

2014 ◽  
Vol 6 (2) ◽  
pp. 331-338 ◽  
Author(s):  
M. Leirós ◽  
E. Alonso ◽  
M. E. Rateb ◽  
W. E. Houssen ◽  
R. Ebel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Primary Cortical Neurons

scholarly journals Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer’s disease related pathology

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Amit U. Joshi ◽  
Lauren D. Van Wassenhove ◽  
Kelsey R. Logas ◽  
Paras S. Minhas ◽  
Katrin I. Andreasson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Alcohol Consumption ◽  
Mitochondrial Dysfunction ◽  
Aldehyde Dehydrogenase ◽  
Cortical Neurons ◽  
Aldehyde Dehydrogenase 2 ◽  
East Asians

AbstractAldehyde dehydrogenase 2 deficiency (ALDH2*2) causes facial flushing in response to alcohol consumption in approximately 560 million East Asians. Recent meta-analysis demonstrated the potential link between ALDH2*2 mutation and Alzheimer’s Disease (AD). Other studies have linked chronic alcohol consumption as a risk factor for AD. In the present study, we show that fibroblasts of an AD patient that also has an ALDH2*2 mutation or overexpression of ALDH2*2 in fibroblasts derived from AD patients harboring ApoE ε4 allele exhibited increased aldehydic load, oxidative stress, and increased mitochondrial dysfunction relative to healthy subjects and exposure to ethanol exacerbated these dysfunctions. In an in vivo model, daily exposure of WT mice to ethanol for 11 weeks resulted in mitochondrial dysfunction, oxidative stress and increased aldehyde levels in their brains and these pathologies were greater in ALDH2*2/*2 (homozygous) mice. Following chronic ethanol exposure, the levels of the AD-associated protein, amyloid-β, and neuroinflammation were higher in the brains of the ALDH2*2/*2 mice relative to WT. Cultured primary cortical neurons of ALDH2*2/*2 mice showed increased sensitivity to ethanol and there was a greater activation of their primary astrocytes relative to the responses of neurons or astrocytes from the WT mice. Importantly, an activator of ALDH2 and ALDH2*2, Alda-1, blunted the ethanol-induced increases in Aβ, and the neuroinflammation in vitro and in vivo. These data indicate that impairment in the metabolism of aldehydes, and specifically ethanol-derived acetaldehyde, is a contributor to AD associated pathology and highlights the likely risk of alcohol consumption in the general population and especially in East Asians that carry ALDH2*2 mutation.

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