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NecroX-7 prevents oxidative stress-induced cardiomyopathy by inhibition of NADPH oxidase activity in rats
DC Field | Value | Language |
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dc.contributor.author | Park, Joonghoon | - |
dc.contributor.author | Park, Eok | - |
dc.contributor.author | Ahn, Bong-Hyun | - |
dc.contributor.author | Kim, Hyoung Jin | - |
dc.contributor.author | Park, Ji-Hoon | - |
dc.contributor.author | Koo, Sun Young | - |
dc.contributor.author | Kwak, Hyo-Shin | - |
dc.contributor.author | Park, Heui Sul | - |
dc.contributor.author | Kim, Dong Wook | - |
dc.contributor.author | Song, Myoungsub | - |
dc.contributor.author | Yim, Hyeon Joo | - |
dc.contributor.author | Seo, Dong Ook | - |
dc.contributor.author | Kim, Soon Ha | - |
dc.date.accessioned | 2024-05-29T01:30:07Z | - |
dc.date.available | 2024-05-29T01:30:07Z | - |
dc.date.created | 2022-06-20 | - |
dc.date.issued | 2012-08 | - |
dc.identifier.citation | Toxicology and Applied Pharmacology, Vol.263 No.1, pp.1-6 | - |
dc.identifier.issn | 0041-008X | - |
dc.identifier.uri | https://hdl.handle.net/10371/203914 | - |
dc.description.abstract | Oxidative 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.language | 영어 | - |
dc.publisher | Academic Press | - |
dc.title | NecroX-7 prevents oxidative stress-induced cardiomyopathy by inhibition of NADPH oxidase activity in rats | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.taap.2012.05.014 | - |
dc.citation.journaltitle | Toxicology and Applied Pharmacology | - |
dc.identifier.wosid | 000307208900001 | - |
dc.identifier.scopusid | 2-s2.0-84864130358 | - |
dc.citation.endpage | 6 | - |
dc.citation.number | 1 | - |
dc.citation.startpage | 1 | - |
dc.citation.volume | 263 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Park, Joonghoon | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | REACTIVE OXYGEN | - |
dc.subject.keywordPlus | MYOCARDIAL-INFARCTION | - |
dc.subject.keywordPlus | CELL-DEATH | - |
dc.subject.keywordPlus | TERT-BUTYLHYDROPEROXIDE | - |
dc.subject.keywordPlus | CARDIAC-HYPERTROPHY | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | PROMOTES | - |
dc.subject.keywordPlus | NECROSIS | - |
dc.subject.keywordPlus | NOX | - |
dc.subject.keywordPlus | CARDIOTOXICITY | - |
dc.subject.keywordAuthor | NecroX-7 | - |
dc.subject.keywordAuthor | Doxorubicin | - |
dc.subject.keywordAuthor | tert-Butyl hydroperoxide | - |
dc.subject.keywordAuthor | NADPH oxidase | - |
dc.subject.keywordAuthor | Cardiomyopathy | - |
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