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000136376 0247_ $$2doi$$a10.1002/jnr.22754
000136376 0247_ $$2pmid$$apmid:21971686
000136376 0247_ $$2ISSN$$a0360-4012
000136376 0247_ $$2ISSN$$a1097-4547
000136376 037__ $$aDZNE-2020-02698
000136376 041__ $$aEnglish
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000136376 1001_ $$0P:(DE-HGF)0$$aRöhnert, Peter$$b0
000136376 245__ $$aInsufficient endogenous redox buffer capacity may underlie neuronal vulnerability to cerebral ischemia and reperfusion.
000136376 260__ $$aNew York, NY [u.a.]$$bWiley-Liss$$c2012
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000136376 520__ $$aReactive oxygen species (ROS) are key players in ischemia-induced neurodegeneration. We investigated whether hippocampal neurons may lack sufficient redox-buffering capacity to protect against ROS attacks. Using organotypic hippocampal slice cultures (OHSCs) transiently exposed to oxygen and glucose deprivation (OGD) and gerbils suffering from a two-vessel occlusion (2VO) as complementary ex vivo and in vivo models, we have elucidated whether the intrinsic redox systems interfere with ischemia-induced neurodegeneration. Cell- type-specific immunohistological staining of hippocampal slice cultures revealed that pyramidal neurons, in contrast to astrocytes and microglia, express free thiols only weakly. In addition, free thiol levels were extensively decreased throughout the hippocampal formation immediately after OGD, but recovered within 24 hr after reperfusion. In parallel, progressive glia activation and proliferation were observed. Increased neuronal exposure to ROS was monitored by dihydroethidium oxidation in hippocampal pyramidal cell layers immediately after OGD. Coadministration of reduction equivalents (α-lipoic acid) and thiol-stimulating agents (enalapril, ambroxol) decreased ischemia-induced neuronal damage in OGD-treated OHSCs and in gerbils exposed to 2VO, whereas single drug applications remained ineffective. In summary, limited redox buffering capacities of pyramidal neurons may underlie their exceptional vulnerability to cerebral ischemia. Consistently, multidrug treatments supporting endogenous redox systems may offer a strategy to promote valid neuroprotection.
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000136376 650_7 $$2NLM Chemicals$$a(((4-chloromethyl)benzoyl)amino)-tetramethylrhodamine
000136376 650_7 $$2NLM Chemicals$$aFluoresceins
000136376 650_7 $$2NLM Chemicals$$aGlial Fibrillary Acidic Protein
000136376 650_7 $$2NLM Chemicals$$aGlycoproteins
000136376 650_7 $$2NLM Chemicals$$aLectins
000136376 650_7 $$2NLM Chemicals$$aNeuroprotective Agents
000136376 650_7 $$2NLM Chemicals$$aReactive Oxygen Species
000136376 650_7 $$2NLM Chemicals$$aRhodamines
000136376 650_7 $$2NLM Chemicals$$aSulfhydryl Compounds
000136376 650_7 $$2NLM Chemicals$$aisolectin B4-binding glycoprotein, rat
000136376 650_7 $$0104821-25-2$$2NLM Chemicals$$adihydroethidium
000136376 650_7 $$0136832-63-8$$2NLM Chemicals$$a5-chloromethylfluorescein
000136376 650_7 $$073Y7P0K73Y$$2NLM Chemicals$$aThioctic Acid
000136376 650_7 $$0EN464416SI$$2NLM Chemicals$$aEthidium
000136376 650_7 $$0IY9XDZ35W2$$2NLM Chemicals$$aGlucose
000136376 650_2 $$2MeSH$$aAnimals
000136376 650_2 $$2MeSH$$aBrain Ischemia: pathology
000136376 650_2 $$2MeSH$$aCell Death
000136376 650_2 $$2MeSH$$aDisease Models, Animal
000136376 650_2 $$2MeSH$$aEthidium: analogs & derivatives
000136376 650_2 $$2MeSH$$aEthidium: metabolism
000136376 650_2 $$2MeSH$$aFluoresceins: metabolism
000136376 650_2 $$2MeSH$$aGerbillinae
000136376 650_2 $$2MeSH$$aGlial Fibrillary Acidic Protein: metabolism
000136376 650_2 $$2MeSH$$aGlucose: deficiency
000136376 650_2 $$2MeSH$$aGlycoproteins: metabolism
000136376 650_2 $$2MeSH$$aHippocampus: cytology
000136376 650_2 $$2MeSH$$aHypoxia
000136376 650_2 $$2MeSH$$aLectins: metabolism
000136376 650_2 $$2MeSH$$aNeurons: drug effects
000136376 650_2 $$2MeSH$$aNeurons: metabolism
000136376 650_2 $$2MeSH$$aNeurons: pathology
000136376 650_2 $$2MeSH$$aNeuroprotective Agents: pharmacology
000136376 650_2 $$2MeSH$$aOrgan Culture Techniques
000136376 650_2 $$2MeSH$$aOxidation-Reduction
000136376 650_2 $$2MeSH$$aRats
000136376 650_2 $$2MeSH$$aRats, Wistar
000136376 650_2 $$2MeSH$$aReactive Oxygen Species
000136376 650_2 $$2MeSH$$aReperfusion Injury: pathology
000136376 650_2 $$2MeSH$$aRhodamines: metabolism
000136376 650_2 $$2MeSH$$aSulfhydryl Compounds: metabolism
000136376 650_2 $$2MeSH$$aThioctic Acid: pharmacology
000136376 7001_ $$0P:(DE-HGF)0$$aSchröder, Ulrich H$$b1
000136376 7001_ $$0P:(DE-HGF)0$$aZiabreva, Iryna$$b2
000136376 7001_ $$0P:(DE-HGF)0$$aTäger, Michael$$b3
000136376 7001_ $$0P:(DE-HGF)0$$aReymann, Klaus G$$b4
000136376 7001_ $$0P:(DE-2719)9000420$$aStriggow, Frank$$b5$$eLast author$$udzne
000136376 77318 $$2Crossref$$3journal-article$$a10.1002/jnr.22754$$b : Wiley, 2011-10-04$$n1$$p193-202$$tJournal of Neuroscience Research$$v90$$x0360-4012$$y2011
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