Protective effect of L-trans-pyrrolidine-2,4-dicarboxilic acid preload against cell death induced by oxygen/glucose deprivation in differentiated PC12 cells

2005 ◽  
Vol 82 (1) ◽  
pp. 93-102 ◽  
Author(s):  
M. Elena Martín ◽  
Francisco M. Muñoz ◽  
Dale A. Dickinson ◽  
Henry Jay Forman ◽  
Rafael Martín del Río ◽  
...  
Keyword(s):  
Cell Death ◽  
Protective Effect ◽  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Differentiated Pc12 Cells

scholarly journals Protective effect of 20-HETE inhibition in a model of oxygen-glucose deprivation in hippocampal slice cultures

2012 ◽  
Vol 302 (6) ◽  
pp. H1285-H1293 ◽  
Author(s):  
Marija Renic ◽  
Suresh N. Kumar ◽  
Debebe Gebremedhin ◽  
Matthew A. Florence ◽  
Nashaat Z. Gerges ◽  
...  
Keyword(s):  
Cell Death ◽  
Protective Effect ◽  
Caspase 3 ◽  
Hippocampal Slice ◽  
Hippocampal Slices ◽  
Glucose Deprivation ◽  
Dienoic Acid ◽  
Oxygen Glucose Deprivation ◽  
Iodide Uptake ◽  
Hippocampal Slice Cultures

Recent studies have indicated that inhibitors of the synthesis of 20-hydroxyeicosatetraenoic acid (20-HETE) may have direct neuroprotective actions since they reduce infarct volume after ischemia reperfusion in the brain without altering blood flow. To explore this possibility, the present study used organotypic hippocampal slice cultures subjected to oxygen-glucose deprivation (OGD) and reoxygenation to examine whether 20-HETE is released by organotypic hippocampal slices after OGD and whether it contributes to neuronal death through the generation of ROS and activation of caspase-3. The production of 20-HETE increased twofold after OGD and reoxygenation. Blockade of the synthesis of 20-HETE with N-hydroxy- N′-(4-butyl-2-methylphenol)formamidine (HET0016) or its actions with a 20-HETE antagonist, 20-hydroxyeicosa-6( Z),15( Z)-dienoic acid, reduced cell death, as measured by the release of lactate dehydrogenase and propidium iodide uptake. Administration of a 20-HETE mimetic, 20-hydroxyeicosa-5( Z),14( Z)-dienoic acid (5,14-20-HEDE), had the opposite effect and increased injury after OGD. The death of neurons after OGD was associated with an increase in the production of ROS and activation of caspase-3. These effects were attenuated by HET0016 and potentiated after the administration of 5,14-20-HEDE. These findings indicate that the production of 20-HETE by hippocampal slices is increased after OGD and that inhibitors of the synthesis or actions of 20-HETE protect neurons from ischemic cell death. The protective effect of 20-HETE inhibitors is associated with a decrease in superoxide production and activation of caspase-3.

Inhibition of PTEN protects PC12 cells against oxygen-glucose deprivation induced cell death through mitoprotection

2018 ◽  
Vol 1692 ◽  
pp. 100-109 ◽  
Author(s):  
Fereshteh Farajdokht ◽  
Gisou Mohaddes ◽  
Elham Karimi-Sales ◽  
Taiebeh Kafshdooz ◽  
Javad Mahmoudi ◽  
...  
Keyword(s):  
Cell Death ◽  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

Rasagiline, a monoamine oxidase-B inhibitor, protects NGF-differentiated PC12 cells against oxygen-glucose deprivation

1999 ◽  
Vol 58 (3) ◽  
pp. 456-463 ◽  
Author(s):  
Saleh Abu-Raya ◽  
Eran Blaugrund ◽  
Victoria Trembovler ◽  
Eugenia Shilderman-Bloch ◽  
Esther Shohami ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Monoamine Oxidase B ◽  
Differentiated Pc12 Cells
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