Protection of NAD(P)H: Quinone oxidoreductase 1 against renal ischemia/reperfusion injury in mice

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dc.contributor.authorGil Tae Gang-
dc.contributor.authorJung Hwan Hwang-
dc.contributor.authorYong-Hoon Kim-
dc.contributor.authorJung Ran Noh-
dc.contributor.authorKyoung Shim Kim-
dc.contributor.authorJ Y Jeong-
dc.contributor.authorD E Choi-
dc.contributor.authorK W Lee-
dc.contributor.authorJ Y Jung-
dc.contributor.authorM Shong-
dc.contributor.authorChul Ho Lee-
dc.date.accessioned2017-04-19T09:48:01Z-
dc.date.available2017-04-19T09:48:01Z-
dc.date.issued2014-
dc.identifier.issn0891-5849-
dc.identifier.uri10.1016/j.freeradbiomed.2013.10.817ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11729-
dc.description.abstractIschemia/reperfusion (I/R) is the most common cause of acute renal injury. I/R-induced reactive oxygen species (ROS) are thought to be a major factor in the development of acute renal injury by promoting the initial tubular damage. NAD(P)H:quinone oxidoreductase 1 (NQO1) is a well-known antioxidant protein that regulates ROS generation. The purpose of this study was to investigate whether NQO1 modulates the renal I/R injury (IRI) associated with NADPH oxidase (NOX)-derived ROS production in an animal model. We analyzed renal function, oxidative stress, and tubular apoptosis after IRI. NQO1-/- mice showed increased blood urea nitrogen and creatinine levels, tubular damage, oxidative stress, and apoptosis. In the kidneys of NQO1-/- mice, the cellular NADPH/NADP+ ratio was significantly higher and NOX activity was markedly higher than in those of NQO1+/+ mice. The activation of NQO1 by β-lapachone (βL) significantly improved renal dysfunction and reduced tubular cell damage, oxidative stress, and apoptosis by renal I/R. Moreover, the βL treatment significantly lowered the cellular NADPH/NADP+ ratio and dramatically reduced NOX activity in the kidneys after IRI. From these results, it was concluded that NQO1 has a protective role against renal injury induced by I/R and that this effect appears to be mediated by decreased NOX activity via cellular NADPH/NADP+ modulation. These results provide convincing evidence that NQO1 activation might be beneficial for ameliorating renal injury induced by I/R.-
dc.publisherElsevier-
dc.titleProtection of NAD(P)H: Quinone oxidoreductase 1 against renal ischemia/reperfusion injury in mice-
dc.title.alternativeProtection of NAD(P)H: Quinone oxidoreductase 1 against renal ischemia/reperfusion injury in mice-
dc.typeArticle-
dc.citation.titleFree Radical Biology and Medicine-
dc.citation.number1-
dc.citation.endPage149-
dc.citation.startPage139-
dc.citation.volume67-
dc.contributor.affiliatedAuthorGil Tae Gang-
dc.contributor.affiliatedAuthorJung Hwan Hwang-
dc.contributor.affiliatedAuthorYong-Hoon Kim-
dc.contributor.affiliatedAuthorJung Ran Noh-
dc.contributor.affiliatedAuthorKyoung Shim Kim-
dc.contributor.affiliatedAuthorChul Ho Lee-
dc.contributor.alternativeName강길태-
dc.contributor.alternativeName황정환-
dc.contributor.alternativeName김용훈-
dc.contributor.alternativeName노정란-
dc.contributor.alternativeName김경심-
dc.contributor.alternativeName정진영-
dc.contributor.alternativeName최대은-
dc.contributor.alternativeName이강욱-
dc.contributor.alternativeName정주영-
dc.contributor.alternativeName송민호-
dc.contributor.alternativeName이철호-
dc.identifier.bibliographicCitationFree Radical Biology and Medicine, vol. 67, no. 1, pp. 139-149-
dc.identifier.doi10.1016/j.freeradbiomed.2013.10.817-
dc.subject.keywordβ-Lapachone-
dc.subject.keywordFree radicals-
dc.subject.keywordIschemia/reperfusion injury-
dc.subject.keywordNADPH oxidase-
dc.subject.keywordNQO1-
dc.subject.localβ-lapachone-
dc.subject.localβ-Lapachone-
dc.subject.localfree radicals-
dc.subject.localFree radicals-
dc.subject.localfree radical-
dc.subject.localIschemia/reperfusion injury-
dc.subject.localNADPH oxidase-
dc.subject.localNQO1-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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