Chondroitin sulfate reduces cell death of rat hippocampal slices subjected to oxygen and glucose deprivation by inhibiting p38, NFκB and iNOS

2011 ◽  
Vol 58 (6) ◽  
pp. 676-683 ◽  
Author(s):  
María Dolores Martín-de-Saavedra ◽  
Laura del Barrio ◽  
Noelia Cañas ◽  
Javier Egea ◽  
Silvia Lorrio ◽  
...  
Keyword(s):  
Cell Death ◽  
Chondroitin Sulfate ◽  
Hippocampal Slices ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation

scholarly journals High-density lipoprotein protects cardiomyocytes against necrosis induced by oxygen and glucose deprivation through SR-B1, PI3K, and AKT1 and 2

2018 ◽  
Vol 475 (7) ◽  
pp. 1253-1265 ◽  
Author(s):  
Kristina K. Durham ◽  
Kevin M. Chathely ◽  
Bernardo L. Trigatti
Keyword(s):  
Cell Death ◽  
High Density Lipoprotein ◽  
Ischemia Reperfusion ◽  
Density Lipoprotein ◽  
Glucose Deprivation ◽  
High Density ◽  
Dependent Manner ◽  
Protective Effects ◽  
Oxygen And Glucose Deprivation ◽  
Ventricular Cardiomyocytes

The cardioprotective lipoprotein HDL (high-density lipoprotein) prevents myocardial infarction and cardiomyocyte death due to ischemia/reperfusion injury. The scavenger receptor class B, type 1 (SR-B1) is a high-affinity HDL receptor and has been shown to mediate HDL-dependent lipid transport as well as signaling in a variety of different cell types. The contribution of SR-B1 in cardiomyocytes to the protective effects of HDL on cardiomyocyte survival following ischemia has not yet been studied. Here, we use a model of simulated ischemia (oxygen and glucose deprivation, OGD) to assess the mechanistic involvement of SR-B1, PI3K (phosphatidylinositol-3-kinase), and AKT in HDL-mediated protection of cardiomyocytes from cell death. Neonatal mouse cardiomyocytes and immortalized human ventricular cardiomyocytes, subjected to OGD for 4 h, underwent substantial cell death due to necrosis but not necroptosis or apoptosis. Pretreatment of cells with HDL, but not low-density lipoprotein, protected them against OGD-induced necrosis. HDL-mediated protection was lost in cardiomyocytes from SR-B1−/− mice or when SR-B1 was knocked down in human immortalized ventricular cardiomyocytes. HDL treatment induced the phosphorylation of AKT in cardiomyocytes in an SR-B1-dependent manner. Finally, chemical inhibition of PI3K or AKT or silencing of either AKT1 or AKT2 gene expression abolished HDL-mediated protection against OGD-induced necrosis of cardiomyocytes. These results are the first to identify a role of SR-B1 in mediating the protective effects of HDL against necrosis in cardiomyocytes, and to identify AKT activation downstream of SR-B1 in cardiomyocytes.

scholarly journals Molecular and Pharmacological Modulation of CALHM1 Promote Neuroprotection against Oxygen and Glucose Deprivation in a Model of Hippocampal Slices

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 664 ◽  
Author(s):  
Javier Garrosa ◽  
Iñigo Paredes ◽  
Philippe Marambaud ◽  
Manuela G. López ◽  
María F. Cano-Abad
Keyword(s):  
Neuroprotective Effect ◽  
Hippocampal Slices ◽  
Glucose Deprivation ◽  
Point Of View ◽  
Oxygen And Glucose Deprivation ◽  
Molecular Events ◽  
Vitro Model ◽  
Species Production ◽  
Reperfusion Phase

Calcium homeostasis modulator 1 (CALHM1) is a calcium channel involved in the regulation of cytosolic Ca2+ levels. From a physiological point of view, the open state of CALHM1 depends not only on voltage but also on the extracellular concentration of calcium ([Ca2+]) ions. At low [Ca2+]e or depolarization, the channel is opened, allowing Ca2+ influx; however, high extracellular [Ca2+]e or hyperpolarization promote its resting state. The unique Ca2+ permeation of CALHM1 relates to the molecular events that take place in brain ischemia, such as depolarization and extracellular changes in [Ca2+]e, particularly during the reperfusion phase after the ischemic insult. In this study, we attempted to understand its role in an in vitro model of ischemia, namely oxygen and glucose deprivation, followed by reoxygenation (OGD/Reox). To this end, hippocampal slices from wild-type Calhm1+/+, Calhm1+/−, and Calhm1−/− mice were subjected to OGD/Reox. Our results point out to a neuroprotective effect when CALHM1 is partially or totally absent. Pharmacological manipulation of CALHM1 with CGP37157 reduced cell death in Calhm1+/+ slices but not in that of Calhm1−/− mice after exposure to the OGD/Reox protocol. This ionic protection was also verified by measuring reactive oxygen species production upon OGD/Reox in Calhm1+/+ and Calhm1−/− mice, resulting in a downregulation of ROS production in Calhm1−/− hippocampal slices and increased expression of HIF-1α. Taken together, we can conclude that genetic or pharmacological inhibition of CALHM1 results in a neuroprotective effect against ischemia, due to an attenuation of the neuronal calcium overload and downregulation of oxygen reactive species production.

scholarly journals Guanosine controls inflammatory pathways to afford neuroprotection of hippocampal slices under oxygen and glucose deprivation conditions

2013 ◽  
Vol 126 (4) ◽  
pp. 437-450 ◽  
Author(s):  
Tharine Dal-Cim ◽  
Fabiana K. Ludka ◽  
Wagner C. Martins ◽  
Charlise Reginato ◽  
Esther Parada ◽  
...  
Keyword(s):  
Hippocampal Slices ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Inflammatory Pathways

scholarly journals Purine receptors are required for DHA-mediated neuroprotection against oxygen and glucose deprivation in hippocampal slices

2014 ◽  
Vol 11 (1) ◽  
pp. 117-126 ◽  
Author(s):  
Simone Molz ◽  
Gislaine Olescowicz ◽  
Jessica Rossana Kraus ◽  
Fabiana Kalyne Ludka ◽  
Carla I. Tasca
Keyword(s):  
Hippocampal Slices ◽  
Glucose Deprivation ◽  
Purine Receptors ◽  
Oxygen And Glucose Deprivation

Postconditioning mitigates cell death following oxygen and glucose deprivation in PC12 cells and forebrain reperfusion injury in rats

2014 ◽  
Vol 93 (1) ◽  
pp. 140-148 ◽  
Author(s):  
Han-Chen Lin ◽  
Purnima Narasimhan ◽  
Shin-Yun Liu ◽  
Pak H. Chan ◽  
I-Rue Lai
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation

Overexpression of bcl-xLProtects Astrocytes from Glucose Deprivation and Is Associated with Higher Glutathione, Ferritin, and Iron Levels 

1999 ◽  
Vol 91 (4) ◽  
pp. 1036-1036 ◽  
Author(s):  
Lijun Xu ◽  
Iphigenia L. Koumenis ◽  
Jonathan L. Tilly ◽  
Rona G. Giffard
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Glucose Deprivation ◽  
Normal Brain ◽  
Oxygen And Glucose Deprivation ◽  
Area Of Interest ◽  
Primary Astrocyte ◽  
Cell Death Gene ◽  
Antioxidant Effects ◽  
Normal Brain Development

Background The possibility of altering outcome from ischemia-like injury by overexpressing the anti-cell death gene bcl-xL was studied. Cells are known to die by different pathways including apoptosis, or programmed cell death, and necrosis. The bcl-xL gene is a member of a family of apoptosis regulating genes and often displays the death-inhibiting properties of the prototype of this family, bcl-2. It is of special interest to study bcl-xL for possible brain protection, because, unlike bcl-2, it is important for normal brain development. Methods Overexpression of bcl-xL was achieved in primary astrocyte cultures using a retroviral vector. Cultures of astrocytes overexpressing bcl-xL or a control gene were injured by hydrogen peroxide, glucose deprivation, or combined oxygen and glucose deprivation. Outcome was assessed morphologically and by release of lactate dehydrogenase. We assessed antioxidant effects by measuring glutathione using monochlorobimane, ferritin by immunoblotting, the level of iron spectrophotometrically, and superoxide using iodonitrotetrazolium violet and dihydroethidium. Results Protection by bcl-xL was found against glucose deprivation and hydrogen peroxide exposure but not combined oxygen and glucose deprivation. Higher levels of superoxide were found, without increased levels of lipid peroxidation. Overexpression of bcl-xL was associated with elevated glutathione levels, elevated ferritin levels, and increased amounts of iron. The increased glutathione contributed to the protection from glucose deprivation. Conclusions Overexpression of bcl-xL protects astrocytes from oxidative injury with the same spectrum of protection seen previously for bcl-2. The increased antioxidant defense observed should be beneficial against both apoptotic and necrotic cell death. The effects on levels of ferritin and iron are novel and identify a new area of interest for this gene family. Whether this relates to the effects of these genes on mitochondrial function remains to be elucidated.

Acute and repeated restraint stress influences cellular damage in rat hippocampal slices exposed to oxygen and glucose deprivation

2005 ◽  
Vol 65 (5) ◽  
pp. 443-450 ◽  
Author(s):  
Fernanda Urruth Fontella ◽  
Helena Cimarosti ◽  
Leonardo Machado Crema ◽  
Ana Paula Thomazi ◽  
Marina Concli Leite ◽  
...  
Keyword(s):  
Restraint Stress ◽  
Hippocampal Slices ◽  
Glucose Deprivation ◽  
Cellular Damage ◽  
Oxygen And Glucose Deprivation ◽  
Repeated Restraint Stress ◽  
Stress Influences
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