scholarly journals Reappraisal of anoxic spreading depolarization as a terminal event during oxygen–glucose deprivation in brain slices in vitro

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Elvira Juzekaeva ◽  
Azat Gainutdinov ◽  
Marat Mukhtarov ◽  
Roustem Khazipov
Keyword(s):  
Membrane Potential ◽  
Brain Slices ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Terminal Event ◽  
Irreversible Damage ◽  
Neuronal Viability ◽  
Spreading Depolarization ◽  
Cortical Slices

Abstract Anoxic spreading depolarization (aSD) has been hypothesized as a terminal event during oxygen–glucose deprivation (OGD) in submerged cortical slices in vitro. However, mechanical artifacts caused by aSD-triggered edema may introduce error in the assessment of neuronal viability. Here, using continuous patch-clamp recordings from submerged rat cortical slices, we first confirmed that vast majority of L4 neurons permanently lost their membrane potential during OGD-induced aSD. In some recordings, spontaneous transition from whole-cell to out-side out configuration occurred during or after aSD, and only a small fraction of neurons survived aSD with reperfusion started shortly after aSD. Secondly, to minimize artifacts caused by OGD-induced edema, cells were short-term patched following OGD episodes of various duration. Nearly half of L4 cells maintained membrane potential and showed the ability to spike-fire if reperfusion started less than 10 min after aSD. The probability of finding live neurons progressively decreased at longer reperfusion delays at a rate of about 2% per minute. We also found that neurons in L2/3 show nearly threefold higher resistance to OGD than neurons in L4. Our results suggest that in the OGD ischemia model, aSD is not a terminal event, and that the “commitment point” of irreversible damage occurs at variable delays, in the range of tens of minutes, after OGD-induced aSD in submerged cortical slices.

Immature rat brain slices exposed to oxygen–glucose deprivation as an in vitro model of neonatal hypoxic–ischemic encephalopathy

2005 ◽  
Vol 145 (1-2) ◽  
pp. 205-212 ◽  
Author(s):  
David Fernández-López ◽  
José Martínez-Orgado ◽  
Ignacio Casanova ◽  
Bartolomé Bonet ◽  
Juan Carlos Leza ◽  
...  
Keyword(s):  
Rat Brain ◽  
In Vitro Model ◽  
Brain Slices ◽  
Glucose Deprivation ◽  
Hypoxic Ischemic Encephalopathy ◽  
Oxygen Glucose Deprivation ◽  
Immature Rat ◽  
Vitro Model ◽  
Ischemic Encephalopathy

scholarly journals A New Brominated Norsesquiterpene Glycoside From the Rhizomes of Acorus tatarinowii Schott

2021 ◽  
Vol 16 (2) ◽  
pp. 1934578X2199226
Author(s):  
Zhi-You Hao ◽  
Gang Ni ◽  
Dong Liang ◽  
Yan-Fei Liu ◽  
Chun-Lei Zhang ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Magnetic Resonance ◽  
Pc12 Cells ◽  
Absolute Configuration ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
In Vitro Tests ◽  
Nuclear Magnetic Resonance Spectra ◽  
Acorus Tatarinowii

A new brominated norsesquiterpene glycoside, acoruside (1), has been isolated from the rhizomes of Acorus tatarinowii Schott, together with 8 known compounds (2-9). Their structures were elucidated mainly based on 1-dimensional (1D) and 2D nuclear magnetic resonance spectra. The absolute configuration of compound 1 was determined by comparing its experimental and calculated electronic circular dichroism spectra. The in vitro tests indicated that at 10 µM, compounds 2, 3, and 4 aggravated serum deprivation injuries of PC12 cells, compound 2 aggravated rotenone-induced injuries of PC12 cells, and compounds 3 and 4 aggravated the oxygen-glucose deprivation-induced injuries of PC12 cells.

scholarly journals Synthesis, Neuroprotection, and Antioxidant Activity of 1,1′-Biphenylnitrones as α-Phenyl-N-tert-butylnitrone Analogues in In Vitro Ischemia Models

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1127 ◽  
Author(s):  
Beatriz Chamorro ◽  
David García-Vieira ◽  
Daniel Diez-Iriepa ◽  
Estíbaliz Garagarza ◽  
Mourad Chioua ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Antioxidant Activities ◽  
Antioxidant Properties ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Human Neuroblastoma ◽  
In Vitro Ischemia ◽  
Lipoxygenase Inhibition ◽  
Antioxidant Agent

Herein, we report the neuroprotective and antioxidant activity of 1,1′-biphenyl nitrones (BPNs) 1–5 as α-phenyl-N-tert-butylnitrone analogues prepared from commercially available [1,1′-biphenyl]-4-carbaldehyde and [1,1′-biphenyl]-4,4′-dicarbaldehyde. The neuroprotection of BPNs1-5 has been measured against oligomycin A/rotenone and in an oxygen–glucose deprivation in vitro ischemia model in human neuroblastoma SH-SY5Y cells. Our results indicate that BPNs 1–5 have better neuroprotective and antioxidant properties than α-phenyl-N-tert-butylnitrone (PBN), and they are quite similar to N-acetyl-L-cysteine (NAC), which is a well-known antioxidant agent. Among the nitrones studied, homo-bis-nitrone BPHBN5, bearing two N-tert-Bu radicals at the nitrone motif, has the best neuroprotective capacity (EC50 = 13.16 ± 1.65 and 25.5 ± 3.93 μM, against the reduction in metabolic activity induced by respiratory chain blockers and oxygen–glucose deprivation in an in vitro ischemia model, respectively) as well as anti-necrotic, anti-apoptotic, and antioxidant activities (EC50 = 11.2 ± 3.94 μM), which were measured by its capacity to reduce superoxide production in human neuroblastoma SH-SY5Y cell cultures, followed by mononitrone BPMN3, with one N-Bn radical, and BPMN2, with only one N-tert-Bu substituent. The antioxidant activity of BPNs1-5 has also been analyzed for their capacity to scavenge hydroxyl free radicals (82% at 100 μM), lipoxygenase inhibition, and the inhibition of lipid peroxidation (68% at 100 μM). Results showed that although the number of nitrone groups improves the neuroprotection profile of these BPNs, the final effect is also dependent on the substitutent that is being incorporated. Thus, BPNs bearing N-tert-Bu and N-Bn groups show better neuroprotective and antioxidant properties than those substituted with Me. All these results led us to propose homo-bis-nitrone BPHBN5 as the most balanced and interesting nitrone based on its neuroprotective capacity in different neuronal models of oxidative stress and in vitro ischemia as well as its antioxidant activity.

Effect of Ischemia In vivo and Oxygen-Glucose Deprivation In vitro on NOS Pools in the Spinal Cord: Comparative Study

2006 ◽  
Vol 26 (7-8) ◽  
pp. 1279-1292 ◽  
Author(s):  
Mária Kolesárová ◽  
Jaroslav Pavel ◽  
Nadežda Lukáčová ◽  
Dalibor Kolesár ◽  
Jozef Maršala
Keyword(s):  
Spinal Cord ◽  
Comparative Study ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

scholarly journals MicroRNA-429/Cxcl1 Axis Protective Against Oxygen Glucose Deprivation/Reoxygenation-Induced Injury in Brain Microvascular Endothelial Cells

Dose-Response ◽  
2020 ◽  
Vol 18 (2) ◽  
pp. 155932582091378
Author(s):  
Jun Leng ◽  
Wei Liu ◽  
Li Li ◽  
Fang Yue Wei ◽  
Meng Tian ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Luciferase Reporter ◽  
Microvascular Endothelial Cells ◽  
Oxygen Glucose Deprivation ◽  
Brain Microvascular Endothelial Cells ◽  
Public Data ◽  
Microvascular Endothelial

Objective: The objective of the present work was to study the role of Cxcl1 in cerebral ischemia–reperfusion (I/R) injury and to in-depth explore its pathogenesis. Methods: The expression of Cxcl1 based on the public data was analyzed. Then, we constructed an oxygen glucose deprivation/reoxygenation (OGD/R) model in vitro using mice brain microvascular endothelial cells (BMECs) to simulate cerebral I/R in vivo. Results: The results of quantitative real-time polymerase chain reaction assay uncovered that Cxcl1 showed higher expression while miR-429 showed lower expression in BMECs damaged by OGD/R, whereas overexpression of Cxcl1 or inhibition of miR-429 expression can strengthen this effect. Hereafter, through dual luciferase reporter assay, we verified that miR-429 directly targets Cxcl1 and negatively regulates Cxcl1 expression. Furthermore, the results also revealed that overexpression of Cxcl1 can reverse the miR-429-mediated effects. Conclusion: We concluded that miR-429 exerts protective effects against OGD/R-induce injury in vitro through modulation of Cxcl1 and nuclear factor kinase B pathway, hoping provide a new view on the pathogenesis of cerebral I/R injury and a feasible potential therapeutic target.

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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