scholarly journals Insulin exerts neuroprotection by counteracting the decrease in cell-surface GABAA receptors following oxygen-glucose deprivation in cultured cortical neurons

2005 ◽  
Vol 92 (1) ◽  
pp. 103-113 ◽  
Author(s):  
John G. Mielke ◽  
Yu Tian Wang
Keyword(s):  
Cell Surface ◽  
Gabaa Receptors ◽  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Cultured Cortical Neurons

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.

scholarly journals The cell-permeable mitochondrial calcium uniporter inhibitor Ru265 preserves cortical neuron respiration after lethal oxygen glucose deprivation and reduces hypoxic/ischemic brain injury

2020 ◽  
Vol 40 (6) ◽  
pp. 1172-1181 ◽  
Author(s):  
Robyn J Novorolsky ◽  
Matthew Nichols ◽  
Jong S Kim ◽  
Evgeny V Pavlov ◽  
Joshua J Woods ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cortical Neurons ◽  
Therapeutic Potential ◽  
High Capacity ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Mitochondrial Calcium ◽  
Neuroprotective Effects ◽  
Sensorimotor Deficits ◽  
Cultured Cortical Neurons

The mitochondrial calcium (Ca2+) uniporter (MCU) mediates high-capacity mitochondrial Ca2+ uptake implicated in ischemic/reperfusion cell death. We have recently shown that inducible MCU ablation in Thy1-expressing neurons renders mice resistant to sensorimotor deficits and forebrain neuron loss in a model of hypoxic/ischemic (HI) brain injury. These findings encouraged us to compare the neuroprotective effects of Ru360 and the recently identified cell permeable MCU inhibitor Ru265. Unlike Ru360, Ru265 (2–10 µM) reached intracellular concentrations in cultured cortical neurons that preserved cell viability, blocked the protease activity of Ca2+-dependent calpains and maintained mitochondrial respiration and glycolysis after a lethal period of oxygen–glucose deprivation (OGD). Intraperitoneal (i.p.) injection of adult male C57Bl/6 mice with Ru265 (3 mg/kg) also suppressed HI-induced sensorimotor deficits and brain injury. However, higher doses of Ru265 (10 and 30 mg/kg, i.p.) produced dose-dependent increases in the frequency and duration of seizure-like behaviours. Ru265 is proposed to promote convulsions by reducing Ca2+ buffering and energy production in highly energetic interneurons that suppress brain seizure activity. These findings support the therapeutic potential of MCU inhibition in the treatment of ischemic stroke but also indicate that such clinical translation will require drug delivery strategies which mitigate the pro-convulsant effects of Ru265.

scholarly journals Involvement of Ceramide in Ischemic Tolerance Induced by Preconditioning with Sublethal Oxygen-Glucose Deprivation in Primary Cultured Cortical Neurons of Rats

2010 ◽  
Vol 33 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Mohammad Iqbal Hossain Bhuiyan ◽  
Mohammad Nurul Islam ◽  
Seo Yun Jung ◽  
Hye Hyun Yoo ◽  
Yong Sup Lee ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Ischemic Tolerance ◽  
Oxygen Glucose Deprivation ◽  
Cultured Cortical Neurons

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
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