Search

Your search keyword '"OGD, oxygen-glucose deprivation"' showing total 5 results
Start Over Descriptor "OGD, oxygen-glucose deprivation"
5 results on '"OGD, oxygen-glucose deprivation"'

1. Breast cancer susceptibility protein 1 (BRCA1) rescues neurons from cerebral ischemia/reperfusion injury through NRF2-mediated antioxidant pathway

Author

Hongquan Guo, Xinfeng Liu, Juanji Li, Xiaolei Shi, Yi Xie, Pengfei Xu, Yunzi Li, Qian Liu, Rui Sun, Ye Hong, Mengna Peng, and Gelin Xu

Subjects
0301 basic medicine, BRCT, BRCA1 C-terminal, GPX3, glutathione peroxidase 3, 4-HNE, 4-hydroxynonenol, OGD, oxygen-glucose deprivation, GCLM, glutamate-cysteine ligase regulator subunit, Iba-1, ionized calcium-binding adapter molecule-1, Clinical Biochemistry, SOD1, superoxide dismutase 1, HO-1, heme oxygenase 1, medicine.disease_cause, Biochemistry, NPCs, neural precursor cells, CaMKII, calcium/calmodulin-dependent protein kinase II, Lipid peroxidation, chemistry.chemical_compound, CA1, cornu ammonis 1, NSCs, neural stem cells, 3-NT, 3-nitrotyrosine, XRE, xenobiotic responsive element, skin and connective tissue diseases, lcsh:QH301-705.5, BER, base excision repair, GFP, green fluorescent protein, PSD95, postsynaptic density protein 95, chemistry.chemical_classification, lcsh:R5-920, DCX, doublecortin, ALS, amyotrophic lateral sclerosis, NRF2, nuclear factor (erythroid-derived 2)-like 2, GPX4, glutathione peroxidase 4, 8-OHDG, 8-hydroxy-2′-deoxyguanosine, Signal transduction, lcsh:Medicine (General), Ischemia/Reperfusion, Research Paper, NQO1, NAD(P)H dehydrogenase (quinone 1), DNA damage, DNA repair, Ischemia, I/R, ischemia/reperfusion, CNS, central nervous system, GCLC, glutamate-cysteine ligase catalytic, NRF2, 03 medical and health sciences, ROS, reactive oxygen species, NER, nucleotide excision repair, medicine, MCAO, middle cerebral artery occlusion, SOD2, superoxide dismutase 2, Reactive oxygen species, AD, Alzheimer disease, Organic Chemistry, GFAP, glial fibrillary acidic protein, BRCA1, medicine.disease, ARE, antioxidative response element, 030104 developmental biology, lcsh:Biology (General), chemistry, NHEJ, non-homologous end joining, Oxidative stress, BRCA1, breast cancer susceptibility protein 1, DSBs, double strand breaks, Cancer research, HR, homologous recombination, Reperfusion injury
Abstract

Cellular oxidative stress plays a vital role in the pathological process of neural damage in cerebral ischemia/reperfusion (I/R). The breast cancer susceptibility protein 1 (BRCA1), a tumor suppressor, can modulate cellular antioxidant response and DNA repair. Yet the role of BRCA1 in cerebral I/R injury has not been explored. In this study, we observed that BRCA1 was mainly expressed in neurons and was up-regulated in response to I/R insult. Overexpression of BRCA1 attenuated reactive oxygen species production and lipid peroxidation. Enhanced BRCA1 expression promoted DNA double strand break repair through non-homologous end joining pathway. These effects consequently led to neuronal cell survival and neurological recovery. Mechanically, BRCA1 can interact with the nuclear factor (erythroid-derived 2)-like 2 (NRF2) through BRCA1 C-terminal (BRCT) domain. The cross-talk between BRCT and NRF2 activated the NRF2/Antioxidant Response Element signaling pathway and thus protected injured neurons during cerebral I/R. In conclusion, enhanced BRCA1 after cerebral I/R injury may attenuate or prevent neural damage from I/R via NRF2-mediated antioxidant pathway. The finding may provide a potential therapeutic target against ischemic stroke., Highlights • BRCA1 was up-regulated after cerebral ischemia/reperfusion injury. • Up-regulated BRCA1 attenuated cerebral ischemia/reperfusion injury and cognitive impairment. • BRCA1 binding to NRF2 via BRCT domain triggered NRF2-mediated antioxidant response. • BRCA1 promoted DSBs repair via non-homologous end joining-pathway.

Published
2018
Full Text
View/download PDF

2. Chloride transport inhibitors influence recovery from oxygen–glucose deprivation-induced cellular injury in adult hippocampus

Author

Pond, Brooks B., Galeffi, Francesca, Ahrens, Rebecca, and Schwartz-Bloom, Rochelle D.

Subjects
*CEREBRAL ischemia, *CEREBROVASCULAR disease, *MITOCHONDRIA, *SEA horses
Abstract

Cerebral ischemia in vivo or oxygen–glucose deprivation (OGD) in vitro are characterized by major disturbances in neuronal ionic homeostasis, including significant rises in intracellular Na+, Ca2+, and Cl- and extracellular K+. Recently, considerable attention has been focused on the cation–chloride cotransporters Na–K–Cl cotransporter isoform I (NKCC-1) and K–Cl cotransporter isoform II (KCC2), as they may play an important role in the disruption of ion gradients and subsequent ischemic damage. In this study, we examined the ability of cation–chloride transport inhibitors to influence the biochemical (i.e. ATP) and histological recovery of neurons in adult hippocampal slices exposed to OGD. In the hippocampus, 7 min of OGD caused a loss of ATP that recovered partially (~50%) during 3 h of reoxygenation. Furosemide, which inhibits the NKCC-1 and KCC2 cotransporters, and bumetanide, a more specific NKCC-1 inhibitor, enhanced ATP recovery when measured 3 h after OGD. Furosemide and bumetanide also attenuated area CA1 neuronal injury after OGD. However, higher concentrations of these compounds appear to have additional non-specific toxic effects, limiting ATP recovery following OGD and promoting neuronal injury. The KCC2 cotransporter inhibitor DIOA and the Cl- ATPase inhibitor ethacrynic acid caused neuronal death even in the absence of OGD and promoted cytochrome c release from isolated mitochondria, indicating non-specific toxicities of these compounds. [Copyright &y& Elsevier]

Published
2004
Full Text
View/download PDF

3. Calpain-dependent neurofilament breakdown in anoxic and ischemic rat central axons

Author

Stys, Peter K. and Jiang, Qiubo

Subjects
*CYTOPLASMIC filaments, *CEREBROSPINAL fluid, *HYPOXEMIA, *IMMUNOBLOTTING, *RATS
Abstract

Neurofilaments are key structural components of white matter axons. The effect of in vitro anoxia or oxygen-glucose deprivation (OGD) on the integrity of the 160 and 200 kDa neurofilament isoforms was studied by immunoblot, and correlated with physiological function. Adult rat optic nerves were exposed to 60 min of either anoxia or OGD. Compound action potential area recovered to 22±6% of control after 60 min of anoxia, and to 4±1% after 60 min of OGD. Ca2+-free (+EGTA) perfusate allowed complete recovery after OGD (108±42%). Tetrodotoxin (TTX, 1 μM) was less protective (45±6%). Both anoxia and OGD induced breakdown of neurofilament 160 (NF160) and NF200 revealed by the appearance of multiple lower molecular weight bands mainly in the 75–100 kDa range. Zero-Ca2+/EGTA completely prevented NF breakdown. TTX only partially reduced NF160 degradation. Non-phosphorylated NF200 appeared after reperfusion post-anoxia or OGD, and was also greatly reduced by zero-Ca2+ or TTX. Calpain inhibitors (10 μM calpain inhibitor I or 50 μM MDL 28,170) significantly reduced NF160 and NF200 breakdown/dephosphorylation, but did not improve electrophysiological recovery. Significant calpain-mediated breakdown of NF160 and NF200 indicates structural damage to the axonal cytoskeleton, which was completely Ca2+-dependent. While pharmacological inhibition of calpain alone greatly reduced NF proteolysis, there was no concomitant improvement in function. These results imply that calpain inhibition is necessary but not sufficient for white matter protection, and emphasize the existence of multiple Ca2+-dependent degradative pathways activated in injured white matter. [Copyright &y& Elsevier]

Published
2002
Full Text
View/download PDF

4. Ameliorating effects of traditional Chinese medicine preparation, Chinese materia medica and active compounds on ischemia/reperfusion-induced cerebral microcirculatory disturbances and neuron damage

Author

Kai Sun, Jing-Yan Han, and Jing-Yu Fan

Subjects
OGD, oxygen-glucose deprivation, MPO, myeloperoxidase, Brain blood barrier, Review, ICAM-1, intercellular adhesion molecule-1, Traditional Chinese medicine, JAM-1, junctional adhesion molecule-1, BNDF, brain-derived neurotrophic factor, ZO-1, zonula occludens-1, Cognitive disabilities, bFGF, basic fibroblast growth factor, ERK, extracellular signal-regulated kinase, GSH, glutathione, RANTES, regulated upon activation normal T-cell expressed and secreted, Asian country, BMEC, brain microvascular endothelial cell, General Pharmacology, Toxicology and Pharmaceutics, IL-8, interleukin-8, ICAM-1, I-κBα, Inhibitory κBα, LDH, lactate dehydrogenase, GRK2, G protein-coupled receptor kinase 2, GSSH, glutathione disulfide, HE, hematoxylin and eosin, Cav-1, caveolin-1, IL-10, interleukin-10, TTC, 2,3,5-triphenyltetrazolium chloride, Hyperpermeability, I/R, ischemia-reperfusion, VEGF, vascular endothelial growth factor, cAMP, cyclic adenosine monophosphate, HIF, hypoxia-inducible factor, medicine.anatomical_structure, HPLC, high performance liquid chromatography, COX-2, cyclooxygenase-2, JNK, Jun N-terminal kinase, iNOS, inducible nitric oxide synthase, TBARS, thiobarbituric acid reactive substance, Cardiology, Antioxidant, CBF, cerebral blood flow, TCM, traditional Chinese medicine, Gly, glysine, AIF, apoptosis inducing factor, Perfusion, AP-1, activator protein-1, PARP, poly-ADP-ribose polymerase, Asp, aspartate, medicine.medical_specialty, AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, GSH-Px, glutathione peroxidase, IL-1β, interleukin-1β, NGF, nerve growth factor, rtPA, recombinant tissue plasminogen activator, Ischemia, Materia medica, Ischemia/reperfusion, PMN, polymorphonuclear, BBB, brain blood barrier, 8-OHdG, 8-hydroxydeoxyguanosine, ROS, reactive oxygen species, SOD, superoxide dismutase, Internal medicine, VCAM-1, vascular adhesion molecule-1, medicine, NMDA, N-methyl-d-aspartic acid, NSC, neural stem cells, MCAO, middle cerebral artery occlusion, TNF-α, tissue necrosis factor-α, MDA, malondialdehyde, NO, nitric oxide, Glu, glutamate, business.industry, lcsh:RM1-950, TGF-β1, transforming growth factor β1, Neuron, NADPH, nicotinamide adenine dinucleotide phosphate, NF-κB, nuclear factor κ-B, medicine.disease, Tuj-1, class III β-tublin, hs-CRP, high-sensitivity C-reactive protein, lcsh:Therapeutics. Pharmacology, TIMP-1, tissue inhibitor of metalloproteinase-1, Leukocyte adhesion, TUNEL, terminal-deoxynucleoitidyl transferase mediated nick end labeling, Immunology, MMPs, matrix metalloproteinases, DPPH, 1,1-diphenyl-2-picrylhydrazyl radical 2,2-diphenyl-1-(2,4,6-trinitrophenyl) hydrazyl, CAT, catalase, business, DHR, dihydrorhodamine 123, GABA, γ-aminobutyric acid, MRI, magnetic resonance imaging, MAPK, mitogen activated protein kinase, SFDA, state food and drug administration
Abstract

Ischemic stroke and ischemia/reperfusion (I/R) injury induced by thrombolytic therapy are conditions with high mortality and serious long-term physical and cognitive disabilities. They have a major impact on global public health. These disorders are associated with multiple insults to the cerebral microcirculation, including reactive oxygen species (ROS) overproduction, leukocyte adhesion and infiltration, brain blood barrier (BBB) disruption, and capillary hypoperfusion, ultimately resulting in tissue edema, hemorrhage, brain injury and delayed neuron damage. Traditional Chinese medicine (TCM) has been used in China, Korea, Japan and other Asian countries for treatment of a wide range of diseases. In China, the usage of compound TCM preparation to treat cerebrovascular diseases dates back to the Han Dynasty. Even thousands of years earlier, the medical formulary recorded many classical prescriptions for treating cerebral I/R-related diseases. This review summarizes current information and underlying mechanisms regarding the ameliorating effects of compound TCM preparation, Chinese materia medica, and active components on I/R-induced cerebral microcirculatory disturbances, brain injury and neuron damage., Graphical abstract TCM preparation, Chinese materia medica and their active compounds show potential to ameliorate I/R-induced cerebral microcirculatory disturbances, brain injury and neuron damage with anti-inflammation, anti-oxidation, anti-apoptosis, anti-excitoxicity and pro-neurogenesis as the major underlying mechanisms.

Published
2015
Full Text
View/download PDF

5. Sex-Specific Activation of Cell Death Signalling Pathways in Cerebellar Granule Neurons Exposed to Oxygen Glucose Deprivation Followed by Reoxygenation

Author

Jaswinder Sharma, Michael V. Johnston, Mary Ann Wilson, Mir Ahamed Hossain, and Geetha Nelluru

Subjects
Male, OGD, oxygen-glucose deprivation, Poly (ADP-Ribose) Polymerase-1, Mice, Adenosine Triphosphate, 0302 clinical medicine, caspase 8, Cerebellum, caspase 3, MB, mitochondrial buffer, Caspase, Mice, Knockout, Neurons, Sex Characteristics, 0303 health sciences, LDH, lactate dehydrogenase, Cell Death, biology, General Neuroscience, Cytochrome c, apoptosis, DIV 9, 9 days in vitro, HRP, horseradish peroxidase, Apoptosis Inducing Factor, neuronal death, S11, Mitochondria, Cell biology, AM: acetoxymethyl ester, VDAC, voltage-dependent anion channel, Hypoxia-Ischemia, Brain, Apoptosis-inducing factor, Female, HI, hypoxia–ischaemia, Poly(ADP-ribose) Polymerases, Research Article, Signal Transduction, Programmed cell death, Cyt C, cytochrome c, hypoxia–ischaemia, Poly ADP ribose polymerase, Caspase 3, S3, Caspase 8, lcsh:RC321-571, PI, propidium iodide, 03 medical and health sciences, Animals, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, 030304 developmental biology, KO, knockout, pNA, p-nitroaniline, HBSS, Hanks' balanced salt solution, Parp-1/PARP-1, poly(ADP-ribose) polymerase-1, WT, wild-type, Reox, reoxygenation, TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling, AIF, apoptosis-inducing factor, CGN, cerebellar granule neuron, Oxygen, Glucose, nervous system, Apoptosis, sexual dimorphism, biology.protein, Neurology (clinical), 030217 neurology & neurosurgery, DAPI, 4′,6-diamidino-2-phenylindole
Abstract

Neuronal death pathways following hypoxia–ischaemia are sexually dimorphic, but the underlying mechanisms are unclear. We examined cell death mechanisms during OGD (oxygen-glucose deprivation) followed by Reox (reoxygenation) in segregated male (XY) and female (XX) mouse primary CGNs (cerebellar granule neurons) that are WT (wild-type) or Parp-1 [poly(ADP-ribose) polymerase 1] KO (knockout). Exposure of CGNs to OGD (1.5 h)/Reox (7 h) caused cell death in XY and XX neurons, but cell death during Reox was greater in XX neurons. ATP levels were significantly lower after OGD/Reox in WT-XX neurons than in XY neurons; this difference was eliminated in Parp-1 KO-XX neurons. AIF (apoptosis-inducing factor) was released from mitochondria and translocated to the nucleus by 1 h exclusively in WT-XY neurons. In contrast, there was a release of Cyt C (cytochrome C) from mitochondria in WT-XX and Parp-1 KO neurons of both sexes; delayed activation of caspase 3 was observed in the same three groups. Thus deletion of Parp-1 shunted cell death towards caspase 3-dependent apoptosis. Delayed activation of caspase 8 was also observed in all groups after OGD/Reox, but was much greater in XX neurons, and caspase 8 translocated to the nucleus in XX neurons only. Caspase 8 activation may contribute to increased XX neuronal death during Reox, via caspase 3 activation. Thus, OGD/Reox induces death of XY neurons via a PARP-1-AIF-dependent mechanism, but blockade of PARP-1-AIF pathway shifts neuronal death towards a caspase-dependent mechanism. In XX neurons, OGD/Reox caused prolonged depletion of ATP and delayed activation of caspase 8 and caspase 3, culminating in greater cell death during Reox.

Published
2011
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results