Attenuation of Neuronal Death by NMDA and Oxygen-Glucose Deprivation in Cortical Neurons Maintained in High Glucose

1999 ◽  
Vol 893 (1 OXIDATIVE/ENE) ◽  
pp. 396-399 ◽  
Author(s):  
SO YOUNG SEO ◽  
EUN YOUNG KIM ◽  
HARRIET KIM ◽  
ILO JOU ◽  
BYOUNG JOO GWAG
Keyword(s):  
High Glucose ◽  
Neuronal Death ◽  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

scholarly journals Tissue-Type Plasminogen Activator is Involved in the Process of Neuronal Death Induced by Oxygen–Glucose Deprivation in Culture

2001 ◽  
Vol 21 (6) ◽  
pp. 631-634 ◽  
Author(s):  
Nobuo Nagai ◽  
Seiji Yamamoto ◽  
Takashi Tsuboi ◽  
Hayato Ihara ◽  
Tetsumei Urano ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Neuronal Death ◽  
Cortical Neurons ◽  
Gene Knockout ◽  
Glucose Deprivation ◽  
Tissue Type ◽  
Oxygen Glucose Deprivation ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Cultured Cortical Neurons

Effect of tissue-type plasminogen activator (tPA) on oxygen–glucose deprivation (OGD) was studied in cultured cortical neurons prepared from tPA gene knockout (tPA-KO) and wild-type (Wt) mice. Three hours of OGD induced 45% and 23% of neuronal death in Wt and tPA-KO mice, respectively. Neuronal death in tPA-KO mice was increased to 42% by additional tPA. Six hours of OGD induced 80% and 40% of neuronal death in Wt and tPA-KO mice, respectively, whereas the addition of tPA increased to 62% in tPA-KO mice. These results suggest that tPA is directly involved in the process of neuronal death induced by ischemia-mimic stress without involving vascular or circulatory components.

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 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.

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