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Immobilization stress induces cell death through production of reactive oxygen species in the mouse cerebral cortex.

DC Field Value Language
dc.contributor.authorLee, YJ-
dc.contributor.authorChoi, B-
dc.contributor.authorLee, EH-
dc.contributor.authorChoi, KS-
dc.contributor.authorSohn, S-
dc.date.accessioned2011-04-20T05:04:35Z-
dc.date.available2011-04-20T05:04:35Z-
dc.date.issued2006-
dc.identifier.issn0304-3940-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/2387-
dc.description.abstractProlonged stress has been shown to impair brain function and increase vulnerability to neuronal injury. To elucidate the in vivo response of neuronal cells to induced stress, we immobilized mice by binding their legs. Levels of reactive oxygen species (ROS) in the cerebral cortex were increased after stress induction. NADPH oxidase, interleukin-1beta (IL-1beta) and cyclooxygenase 2 mRNA (COX-2) expression levels were upregulated, and Fas levels were also increased. The increased expression of these factors was associated with neuronal death, which was confirmed by TUNEL and NeuN staining. OX42 staining was also evident around the TUNEL-stained lesions. From these findings, it appears that immobilization stress induces neuronal death in the mouse cerebral cortex, a process mediated by NADPH oxidase, IL-1beta, COX-2, ROS and Fas. However, this could be inhibited by pretreating the animals with antioxidants such as ebselen or pyrrolidine dithiocarbamate.-
dc.language.isoen-
dc.subject.MESHAnalysis of Variance-
dc.subject.MESHAnimals-
dc.subject.MESHAntigens, CD11b/metabolism-
dc.subject.MESHAntigens, CD95/genetics-
dc.subject.MESHAntigens, CD95/metabolism-
dc.subject.MESHAntioxidants/therapeutic use-
dc.subject.MESHAzoles/therapeutic use-
dc.subject.MESHCell Count/methods-
dc.subject.MESHCell Death/drug effects-
dc.subject.MESHCell Death/physiology-
dc.subject.MESHCerebral Cortex/metabolism*-
dc.subject.MESHCerebral Cortex/pathology*-
dc.subject.MESHCyclooxygenase 2/genetics-
dc.subject.MESHCyclooxygenase 2/metabolism-
dc.subject.MESHGene Expression Regulation/physiology-
dc.subject.MESHImmobilization/methods-
dc.subject.MESHImmunohistochemistry/methods-
dc.subject.MESHIn Situ Nick-End Labeling/methods-
dc.subject.MESHInterleukin-1/genetics-
dc.subject.MESHInterleukin-1/metabolism-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred ICR-
dc.subject.MESHNADPH Oxidase/genetics-
dc.subject.MESHNADPH Oxidase/metabolism-
dc.subject.MESHOrganoselenium Compounds/therapeutic use-
dc.subject.MESHPhosphopyruvate Hydratase/metabolism-
dc.subject.MESHRNA, Messenger/biosynthesis-
dc.subject.MESHReactive Oxygen Species/metabolism*-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction/methods-
dc.subject.MESHStress, Physiological/drug therapy-
dc.subject.MESHStress, Physiological/metabolism*-
dc.subject.MESHStress, Physiological/pathology*-
dc.titleImmobilization stress induces cell death through production of reactive oxygen species in the mouse cerebral cortex.-
dc.typeArticle-
dc.identifier.pmid16203091-
dc.identifier.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0304-3940(05)01039-6-
dc.contributor.affiliatedAuthor최, 경숙-
dc.contributor.affiliatedAuthor손, 성향-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.neulet.2005.08.065-
dc.citation.titleNeuroscience letters-
dc.citation.volume392-
dc.citation.number1-2-
dc.citation.date2006-
dc.citation.startPage27-
dc.citation.endPage31-
dc.identifier.bibliographicCitationNeuroscience letters, 392(1-2):27-31, 2006-
dc.identifier.eissn1872-7972-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
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