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Cited 25 time in webofscience Cited 26 time in scopus
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Exposure to electromagnetic field attenuates oxygen-glucose deprivation-induced microglial cell death by reducing intracellular Ca2+ and ROS

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dc.contributor.authorCao Nguyen Duong-
dc.contributor.authorKim, Jae Young-
dc.date.available2020-02-28T02:42:19Z-
dc.date.created2020-02-06-
dc.date.issued2016-04-02-
dc.identifier.issn0955-3002-
dc.identifier.urihttps://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/8375-
dc.description.abstractPurpose The aim of this research was to demonstrate the protective effects of electromagnetic field (EMF) exposure on the human microglial cell line, HMO6, against ischemic cell death induced by in vitro oxygen-glucose deprivation (OGD).Materials and methods HMO6 cells were cultured for 4h under OGD with or without exposure to EMF with different combinations of frequencies and intensities (10, 50, or 100Hz/1mT and 50Hz/0.01, 0.1, or 1mT). Cell survival, intracellular calcium and reactive oxygen species (ROS) levels were measured.Results OGD caused significant HMO6 cell death as well as elevation of intracellular Ca2+ and ROS levels. Among different combinations of EMF frequencies and intensities, 50Hz/1mT EMF was the most potent to attenuate OGD-induced cell death and intracellular Ca2+ and ROS levels. A significant but less potent protective effect was also found at 10Hz/1mT, whereas no protective effect was found at other combinations of EMF. A xanthine oxidase inhibitor reversed OGD-induced ROS production and cell death, while NADPH oxidase and mitochondrial respiration chain complex II inhibitors did not affect cell death.Conclusions 50Hz/1mT EMF protects human microglial cells from OGD-induced cell death by interfering with OGD-induced elevation of intracellular Ca2+ and ROS levels, and xanthine oxidase is one of the main mediators involved in OGD-induced HMO6 cell death. Non-invasive treatment of EMF radiation may be clinically useful to attenuate hypoxic-ischemic brain injury.-
dc.language영어-
dc.language.isoen-
dc.publisherTAYLOR & FRANCIS LTD-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF RADIATION BIOLOGY-
dc.subjectCEREBRAL-ARTERY OCCLUSION-
dc.subjectCORTICAL-NEURONS-
dc.subjectISCHEMIC BRAIN-
dc.subjectNADPH OXIDASE-
dc.subjectNITRIC-OXIDE-
dc.subjectIN-VITRO-
dc.subjectINJURY-
dc.subjectCALCIUM-
dc.subjectMICE-
dc.subjectALLOPURINOL-
dc.titleExposure to electromagnetic field attenuates oxygen-glucose deprivation-induced microglial cell death by reducing intracellular Ca2+ and ROS-
dc.typeArticle-
dc.type.rimsART-
dc.description.journalClass1-
dc.identifier.wosid000371930000003-
dc.identifier.doi10.3109/09553002.2016.1136851-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF RADIATION BIOLOGY, v.92, no.4, pp.195 - 201-
dc.identifier.scopusid2-s2.0-84961123354-
dc.citation.endPage201-
dc.citation.startPage195-
dc.citation.titleINTERNATIONAL JOURNAL OF RADIATION BIOLOGY-
dc.citation.volume92-
dc.citation.number4-
dc.contributor.affiliatedAuthorCao Nguyen Duong-
dc.contributor.affiliatedAuthorKim, Jae Young-
dc.type.docTypeArticle-
dc.subject.keywordAuthorElectromagnetic field-
dc.subject.keywordAuthormicroglia-
dc.subject.keywordAuthorHMO6-
dc.subject.keywordAuthorischemic injury-
dc.subject.keywordAuthorCa2+-
dc.subject.keywordAuthorreactive oxygen species-
dc.subject.keywordPlusCEREBRAL-ARTERY OCCLUSION-
dc.subject.keywordPlusCORTICAL-NEURONS-
dc.subject.keywordPlusISCHEMIC BRAIN-
dc.subject.keywordPlusNADPH OXIDASE-
dc.subject.keywordPlusNITRIC-OXIDE-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordPlusINJURY-
dc.subject.keywordPlusCALCIUM-
dc.subject.keywordPlusMICE-
dc.subject.keywordPlusALLOPURINOL-
dc.relation.journalResearchAreaLife Sciences & Biomedicine - Other Topics-
dc.relation.journalResearchAreaNuclear Science & Technology-
dc.relation.journalResearchAreaRadiology, Nuclear Medicine & Medical Imaging-
dc.relation.journalWebOfScienceCategoryBiology-
dc.relation.journalWebOfScienceCategoryNuclear Science & Technology-
dc.relation.journalWebOfScienceCategoryRadiology, Nuclear Medicine & Medical Imaging-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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