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NecroX-7 prevents oxidative stress-induced cardiomyopathy by inhibition of NADPH oxidase activity in rats

DC Field Value Language
dc.contributor.authorPark, Joonghoon-
dc.contributor.authorPark, Eok-
dc.contributor.authorAhn, Bong-Hyun-
dc.contributor.authorKim, Hyoung Jin-
dc.contributor.authorPark, Ji-Hoon-
dc.contributor.authorKoo, Sun Young-
dc.contributor.authorKwak, Hyo-Shin-
dc.contributor.authorPark, Heui Sul-
dc.contributor.authorKim, Dong Wook-
dc.contributor.authorSong, Myoungsub-
dc.contributor.authorYim, Hyeon Joo-
dc.contributor.authorSeo, Dong Ook-
dc.contributor.authorKim, Soon Ha-
dc.date.accessioned2024-05-29T01:30:07Z-
dc.date.available2024-05-29T01:30:07Z-
dc.date.created2022-06-20-
dc.date.issued2012-08-
dc.identifier.citationToxicology and Applied Pharmacology, Vol.263 No.1, pp.1-6-
dc.identifier.issn0041-008X-
dc.identifier.urihttps://hdl.handle.net/10371/203914-
dc.description.abstractOxidative stress is one of the causes of cardiomyopathy. In the present study, NecroXs, novel class of mitochondrial ROS/RNS scavengers, were evaluated for cardioprotection in in vitro and in vivo model, and the putative mechanism of the cardioprotection of NecroX-7 was investigated by global gene expression profiling and subsequent biochemical analysis. NecroX-7 prevented tert-butyl hydroperoxide (tBHP)-induced death of H9C2 rat cardiomyocytes at EC50=0.057 mu M. In doxorubicin (DOX)-induced cardiomyopathy in rats, NecroX-7 significantly reduced the plasma levels of creatine kinase (CK-MB) and lactate dehydrogenase (LDH) which were increased by DOX treatment (p<0.05). Microarray analysis revealed that 21 genes differentially expressed in tBHP-treated H9C2 cells were involved in 'Production of reactive oxygen species' (p=0.022), and they were resolved by concurrent NecroX-7 treatment. Gene-to-gene networking also identified that NecroX-7 relieved cell death through Ncf1/p47phox and Rac2 modulation. In subsequent biochemical analysis, NecroX-7 inhibited NADPH oxidase (NOX) activity by 53.3% (p<0.001). These findings demonstrate that NecroX-7, in part, provides substantial protection of cardiomyopathy induced by tBHP or DOX via NOX-mediated cell death. (C) 2012 Elsevier Inc. All rights reserved.-
dc.language영어-
dc.publisherAcademic Press-
dc.titleNecroX-7 prevents oxidative stress-induced cardiomyopathy by inhibition of NADPH oxidase activity in rats-
dc.typeArticle-
dc.identifier.doi10.1016/j.taap.2012.05.014-
dc.citation.journaltitleToxicology and Applied Pharmacology-
dc.identifier.wosid000307208900001-
dc.identifier.scopusid2-s2.0-84864130358-
dc.citation.endpage6-
dc.citation.number1-
dc.citation.startpage1-
dc.citation.volume263-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorPark, Joonghoon-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusREACTIVE OXYGEN-
dc.subject.keywordPlusMYOCARDIAL-INFARCTION-
dc.subject.keywordPlusCELL-DEATH-
dc.subject.keywordPlusTERT-BUTYLHYDROPEROXIDE-
dc.subject.keywordPlusCARDIAC-HYPERTROPHY-
dc.subject.keywordPlusINDUCED APOPTOSIS-
dc.subject.keywordPlusPROMOTES-
dc.subject.keywordPlusNECROSIS-
dc.subject.keywordPlusNOX-
dc.subject.keywordPlusCARDIOTOXICITY-
dc.subject.keywordAuthorNecroX-7-
dc.subject.keywordAuthorDoxorubicin-
dc.subject.keywordAuthortert-Butyl hydroperoxide-
dc.subject.keywordAuthorNADPH oxidase-
dc.subject.keywordAuthorCardiomyopathy-
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