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dc.contributor.authorZhou, Dandanen_US
dc.contributor.authorZhuang, Jinqiangen_US
dc.contributor.authorWang, Yihuien_US
dc.contributor.authorZhao, Dandanen_US
dc.contributor.authorZhao, Lidongen_US
dc.contributor.authorZhu, Shunen_US
dc.contributor.authorPu, Jinjunen_US
dc.contributor.authorYin, Mingen_US
dc.contributor.authorZhang, Hongyuen_US
dc.contributor.authorWang, Zejianen_US
dc.contributor.authorHong, Jiangen_US
dc.date.accessioned2020-05-14T14:55:19Z
dc.date.available2020-05-14T14:55:19Z
dc.date.issued2019-03-15
dc.PublishedZhou D, Zhuang, Wang Y, Zhao, Zhao, Zhu, Pu, Yin, Zhang H, Wang, Hong J. Propofol alleviates DNA damage induced by oxygen glucose deprivation and reperfusion via FoxO1 nuclear translocation in H9c2 cells. Frontiers in Physiology. 2019;10:223eng
dc.identifier.issn1664-042X
dc.identifier.urihttps://hdl.handle.net/1956/22280
dc.description.abstractIschemia/reperfusion (I/R) injury induces irreversible oxidative stress damage to the cardiac myocytes. Many studies have revealed that propofol alleviates the important organelle-mediated injury from oxidative stress in vitro. However, it remains unclear whether propofol prevents I/R-induced DNA damage in cardiomyocytes. In our study, we established an oxygen glucose deprivation/reoxygenation (OGD/R) model in H9c2 cells and found that propofol decreased reactive oxygen species (ROS) levels and suppressed cell apoptosis induced by OGD/R in H9c2 cells. In addition, propofol significantly reduced the molecular marker of DNA damage and inhibited double-strand breaks of DNA damage induced by OGD/R in H9c2 cells in a dose-dependent manner. Furthermore, we investigated the molecular mechanisms and demonstrated that propofol inhibited forkhead box O 1 (FoxO1) phosphorylation and increased FoxO1 nuclear translocation through inhibition of protein kinase B (Akt) and adenosine 5’-monophosphate-activated protein kinase (AMPK) pathways. The protective effects of propofol against oxidative stress-induced DNA damage were reversed by silencing FoxO1. Taken together, our results suggest that oxidative stress aggravates DNA damage and apoptosis in H9C2 cells, which can be reversed by propofol via FoxO1 nuclear translocation.en_US
dc.language.isoengeng
dc.publisherFrontierseng
dc.rightsAttribution CC BYeng
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/eng
dc.titlePropofol alleviates DNA damage induced by oxygen glucose deprivation and reperfusion via FoxO1 nuclear translocation in H9c2 cellsen_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2020-01-28T10:20:40Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2019 Zhou, Zhuang, Wang, Zhao, Zhao, Zhu, Pu, Yin, Zhang, Wang and Hong
dc.identifier.doihttps://doi.org/10.3389/fphys.2019.00223
dc.identifier.cristin1768819
dc.source.journalFrontiers in Physiology


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