Oxygen glucose deprivation post-conditioning protects cortical neurons against oxygen-glucose deprivation injury: Role of HSP70 and inhibition of apoptosis

2014 ◽  
Vol 34 (1) ◽  
pp. 18-22 ◽  
Author(s):  
Jian-hua Zhao ◽  
Xian-li Meng ◽  
Jian Zhang ◽  
Yong-li Li ◽  
Yue-juan Li ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

Major role of the PI3K/Akt pathway in ischemic tolerance induced by sublethal oxygen-glucose deprivation in cortical neurons in vitro

2011 ◽  
Vol 34 (6) ◽  
pp. 1023-1034 ◽  
Author(s):  
Mohammad Iqbal Hossain Bhuiyan ◽  
Seo Yun Jung ◽  
Hyoung Ja Kim ◽  
Yong Sup Lee ◽  
Changbae Jin
Keyword(s):  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Ischemic Tolerance ◽  
Akt Pathway ◽  
Oxygen Glucose Deprivation

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 Near infrared radiation rescues mitochondrial dysfunction in cortical neurons after oxygen-glucose deprivation

2014 ◽  
Vol 30 (2) ◽  
pp. 491-496 ◽  
Author(s):  
Zhanyang Yu ◽  
Ning Liu ◽  
Jianhua Zhao ◽  
Yadan Li ◽  
Thomas J. McCarthy ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Infrared Radiation ◽  
Cortical Neurons ◽  
Near Infrared ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Near Infrared Radiation

scholarly journals A natural diarylheptanoid protects cortical neurons against oxygen–glucose deprivation‐induced autophagy and apoptosis

2019 ◽  
Vol 71 (7) ◽  
pp. 1110-1118 ◽  
Author(s):  
Qiaoyun Shi ◽  
Qinghua Zhang ◽  
Yinghui Peng ◽  
Xiaoqi Zhang ◽  
Ying Wang ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

Autophagy triggers endoplasmic reticulum stress and C/EBP homologous protein-mediated apoptosis in OGD/R-treated neurons in a caspase-12-independent manner

2021 ◽  
Author(s):  
Ying Tian ◽  
Liang Wang ◽  
Zhiqiang Qiu ◽  
Yulun Xu ◽  
Rongrong Hua
Keyword(s):  
Endoplasmic Reticulum ◽  
Cortical Neurons ◽  
Neuronal Apoptosis ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Homologous Protein ◽  
Caspase 12 ◽  
Induced Apoptosis

We reported that a high level of autophagy was initiated by oxygen-glucose deprivation (OGD) and was maintained in neurons even after oxygen-glucose deprivation followed by reoxygenation (OGD/R), accompanied by neuronal apoptosis. This study focused on autophagy-induced apoptosis and its signaling network, especially the role of endoplasmic reticulum stress (ERS). Analysis of primary cultured cortical neurons from mice showed that the autophagy-induced apoptosis depended on Caspase-8 and -9 but not Caspase-12. This finding did not mean that the endoplasmic reticulum did not participate in this process. Increases in the levels of endoplasmic reticulum (ER) biomarkers and Binding immunoglobulin protein (BiP) were induced by autophagy in OGD/R-treated neurons. In addition, as an apoptotic transcription factor induced by ER stress, C/EBP homologous protein (CHOP) expression was significantly increased in neurons after OGD/R. This result suggested that the autophagy-Bip-CHOP-caspase (8 and 9)-dependent apoptotic signaling pathway at least partly participated in autophagy-induced apoptosis in primary cortical neurons. It revealed that ER induced apoptosis in neurons suffering from OGD/R injury in an ER stress-CHOP-dependent manner rather than a caspase-12-dependent manner. However, more research on signaling or cross-linking networks and intermediate links are needed. The realization of caspase-12-independent BiP-CHOP neuronal apoptosis pathway has expanded our understanding of the neuronal apoptosis network, which may eventually provide endogenous interventional strategies for OGD/R injury after stroke.

Abstract 144: Role of Iron Metabolism on Outcomes after Cardiac Arrest and Resuscitation in Mice

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Yusuke Miyazaki ◽  
Kei Hayashida ◽  
Takamitsu Ikeda ◽  
Eizo Marutani ◽  
Aranya Bagchi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cardiac Arrest ◽  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Neurological Function ◽  
Lipid Peroxidation Product ◽  
Iron Loading ◽  
Intracellular Iron ◽  
Neurological Outcomes

Introduction: Ischemia and reperfusion (I/R) induces hepcidin in neurons and macrophages. Hepcidin downregulates ferroportin, the only known iron exporter, thereby inhibiting iron efflux and increases iron in ferroportin rich cells while decreasing serum iron. Increased intracellular iron after I/R induces ferroptosis, a regulated cell death characterized by iron-dependent lipid peroxidation. We hypothesized that hepcidin-induced sequestration of iron in neurons and macrophages, both of which express ferroportin, worsens post-cardiac arrest (CA) brain injury. Methods: Levels of hepcidin, iron, and a lipid peroxidation product, malondialdehyde; and expression of HAMP that encodes hepcidin, transferrin receptor 1, and markers of ferroptosis, PTGS2 and CHAC1, were measured in naïve and post-CA wild-type (WT) mice. To examine the effects of hepcidin on CA outcomes, hepcidin-deficient and WT mice were subjected to potassium-induced 8 min of CA followed by cardiopulmonary resuscitation (CPR). To determine the role of increased intracellular iron after CA/CPR, we administered iron-dextran (300 mg/kg IP) or vehicle to WT mice 24h before CA. The effect of liproxstatin-1, a ferroptosis inhibitor, on cell viability was assessed in murine primary cortical neurons after oxygen-glucose deprivation/reperfusion (OGD/R) with iron-loading. Results: Post-CA WT mice exhibited increased systemic HAMP expression, intracellular iron in spleen, and ferroptosis in brain. Hepcidin deficiency that decreases intracellular iron improved survival and neurological function after CA/CPR, whereas pre-arrest iron-loading that increases intracellular iron worsened survival and neurological function after CA/CPR (Fig. 1). Liproxstatin-1 improved neuron viability after OGD/R with iron-loading. Conclusions: Our data suggest that inhibiting hepcidin improves post-CA neurological outcomes by reducing intracellular iron and ferroptosis-induced neuronal death.

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