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dc.contributor.authorSavitree Thummasornen_US
dc.contributor.authorSirinart Kumfuen_US
dc.contributor.authorSiriporn Chattipakornen_US
dc.contributor.authorNipon Chattipakornen_US
dc.date.accessioned2018-09-04T04:06:09Z-
dc.date.available2018-09-04T04:06:09Z-
dc.date.issued2011-05-01en_US
dc.identifier.issn15677249en_US
dc.identifier.other2-s2.0-79953740056en_US
dc.identifier.other10.1016/j.mito.2011.01.008en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=79953740056&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/49723-
dc.description.abstractDuring cardiac ischemia-reperfusion injury, reactive oxygen species (ROS) level is markedly increased, leading to oxidative stress and mitochondrial dysfunction. Although granulocyte-colony stimulating factor (G-CSF) is known to be cardioprotective, its effects on cardiac mitochondria during oxidative stress have never been investigated. In this study, we discovered that G-CSF completely prevented mitochondrial swelling and depolarization, and markedly reduced ROS production caused by H2O2-induced oxidative stress in isolated cardiac mitochondria. Its effects were similar to those treated with cyclosporine A and 4'-chlorodiazepam. These findings suggest that G-CSF could act directly on cardiac mitochondria to prevent mitochondrial dysfunction caused by oxidative stress. © 2011 Elsevier B.V. and Mitochondria Research Society. All rights reserved.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleGranulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondriaen_US
dc.typeJournalen_US
article.title.sourcetitleMitochondrionen_US
article.volume11en_US
article.stream.affiliationsChiang Mai Universityen_US
Appears in Collections:CMUL: Journal Articles

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