Lycopene prevents oxygen-glucose deprivation-induced autophagic death in SH-SY5Y cells via inhibition of the oxidative stress-activated AMPK/mTOR pathway

2021 ◽  
Vol 24 (2) ◽  
Author(s):  
Tan Li ◽  
Yang Zhang ◽  
Yi Qi ◽  
He Liu
Keyword(s):  
Oxidative Stress ◽  
Glucose Deprivation ◽  
Mtor 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 Baicalin attenuates oxygen-glucose deprivation-induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase activation in PC12 cells

2010 ◽  
Vol 31 (2) ◽  
pp. 137-144 ◽  
Author(s):  
Cheng-tan Li ◽  
Wei-ping Zhang ◽  
San-hua Fang ◽  
Yun-bi Lu ◽  
Li-hui Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

scholarly journals Comparative transcriptome of neurons after oxygen–glucose deprivation: Potential differences in neuroprotection versus reperfusion

2018 ◽  
Vol 38 (12) ◽  
pp. 2236-2250 ◽  
Author(s):  
Shuzhen Guo ◽  
Anna Tjärnlund-Wolf ◽  
Wenjun Deng ◽  
Emiri Tejima-Mandeville ◽  
Lauren J Lo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Comparative Transcriptome ◽  
Gene Arrays ◽  
Mk 801 ◽  
Metabolic Inflammation ◽  
Cell Death Pathways ◽  
Rapid Restoration

In the context of ischemic stroke, rescuing neurons can be theoretically achieved with either reperfusion or neuroprotection. Reperfusion works via the rapid restoration of oxygen and glucose delivery. Neuroprotection comprises molecular strategies that seek to block excitotoxicity, oxidative stress or various cell death pathways. Here, we propose the hypothesis that neurons rescued with reperfusion are different from neurons rescued with molecular neuroprotection. Neurons were subjected to oxygen–glucose deprivation (OGD) and then treated with “in vitro reperfusion” (i.e. energetic rescue via restoration of oxygen and glucose) or Z-VADfmk (to block apoptosis) or MK-801 (to block excitotoxicity). Levels of injury were titrated so that equivalent levels of neuronal salvage were achieved with reperfusion or neuroprotection. Gene arrays showed that OGD significantly altered the transcriptomic profiles of surviving neurons. Pathway analysis confirmed that a large spectrum of metabolic, inflammation, and signaling genes were perturbed. In spite of the fact that equal levels of neuronal salvage were achieved, energetic rescue renormalized the transcriptomic profiles in surviving neurons to a larger degree compared to neuroprotection with either Z-VADfmk or MK-801. These findings suggest that upstream reperfusion may bring salvaged neurons back “closer to normal” compared to downstream molecular neuroprotection.

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