Trumbeckaite 2013 Mitochondrion: Difference between revisions
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|abstract=We have introduced a sensitive method for studying oxygen/glucose deprivation (OGD)-induced mitochondrial alterations in homogenates of organotypic hippocampal slice cultures (slices) by high-resolution respirometry. Using this approach, we tested the neuroprotective potential of the novel non-immunosuppressive cyclosporin (CsA) derivative Cs9 in comparison with CsA, the immunosuppressive CsA analogue [D-Ser](8)CsA, and MK 801, a N-methyl-D-aspartate (NMDA) receptor antagonist. OGD/reperfusion reduced the glutamate/malate dependent (and protein-related) state 3 respiration to 30% of its value under control conditions. All of the above drugs reversed this effect, with an increase to >88% of the value for control slices not exposed to OGD. We conclude that Cs9, [D-Ser](8)CsA, and MK 801, despite their different modes of action, protect mitochondria from OGD-induced damage. | |abstract=We have introduced a sensitive method for studying oxygen/glucose deprivation (OGD)-induced mitochondrial alterations in homogenates of organotypic hippocampal slice cultures (slices) by high-resolution respirometry. Using this approach, we tested the neuroprotective potential of the novel non-immunosuppressive cyclosporin (CsA) derivative Cs9 in comparison with CsA, the immunosuppressive CsA analogue [D-Ser](8)CsA, and MK 801, a N-methyl-D-aspartate (NMDA) receptor antagonist. OGD/reperfusion reduced the glutamate/malate dependent (and protein-related) state 3 respiration to 30% of its value under control conditions. All of the above drugs reversed this effect, with an increase to >88% of the value for control slices not exposed to OGD. We conclude that Cs9, [D-Ser](8)CsA, and MK 801, despite their different modes of action, protect mitochondria from OGD-induced damage. | ||
|keywords=Organotypic hippocampal slice cultures; Mitochondria; Cs9; Oxygen/glucose deprivation | |keywords=Organotypic hippocampal slice cultures; Mitochondria; Cs9; Oxygen/glucose deprivation | ||
|mipnetlab=DE Magdeburg Gellerich FN, EE Tartu | |mipnetlab=DE Magdeburg Gellerich FN, EE Tartu Paju K | ||
}} | }} | ||
{{Labeling | {{Labeling |
Revision as of 15:54, 8 June 2015
Trumbeckaite S, Gizatullina Z, Arandarcikaite O, RΓΆhnert P, Vielhaber S, Malesevic M, Fischer G, Seppet E, Striggow F, Gellerich FN (2013) Oxygen glucose deprivation causes mitochondrial dysfunction in cultivated rat hippocampal slices: Protective effects of CsA, its immunosuppressive congener [D-Ser](8)CsA, the novel non-immunosuppressive cyclosporin derivative Cs9, and the NMDA receptor antagonist MK 801. Mitochondrion 13:539β47. |
Trumbeckaite S, Gizatullina Z, Arandarcikaite O, Roehnert P, Vielhaber S, Malesevic M, Fischer G, Seppet E, Striggow F, Gellerich FN (2013) Mitochondrion
Abstract: We have introduced a sensitive method for studying oxygen/glucose deprivation (OGD)-induced mitochondrial alterations in homogenates of organotypic hippocampal slice cultures (slices) by high-resolution respirometry. Using this approach, we tested the neuroprotective potential of the novel non-immunosuppressive cyclosporin (CsA) derivative Cs9 in comparison with CsA, the immunosuppressive CsA analogue [D-Ser](8)CsA, and MK 801, a N-methyl-D-aspartate (NMDA) receptor antagonist. OGD/reperfusion reduced the glutamate/malate dependent (and protein-related) state 3 respiration to 30% of its value under control conditions. All of the above drugs reversed this effect, with an increase to >88% of the value for control slices not exposed to OGD. We conclude that Cs9, [D-Ser](8)CsA, and MK 801, despite their different modes of action, protect mitochondria from OGD-induced damage. β’ Keywords: Organotypic hippocampal slice cultures; Mitochondria; Cs9; Oxygen/glucose deprivation
β’ O2k-Network Lab: DE Magdeburg Gellerich FN, EE Tartu Paju K
Labels:
Stress:Hypoxia, Ischemia-reperfusion;preservation"Ischemia-reperfusion;preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Rat Tissue;cell: Nervous system Preparation: Homogenate Enzyme: Complex I, Complex II;succinate dehydrogenase Regulation: Substrate;glucose;TCA cycle"Substrate;glucose;TCA cycle" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. Coupling state: LEAK, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
HRR: Oxygraph-2k