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Conference Paper: PKC β inhibitor ruboxistaurin prevents the increase of 15-F2t-isoprostane in the myocardium and plasma in Type 1 diabetic rats

TitlePKC β inhibitor ruboxistaurin prevents the increase of 15-F2t-isoprostane in the myocardium and plasma in Type 1 diabetic rats
Authors
KeywordsBiology
Issue Date2010
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2010 Annual Meeting of Experimental Biology (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24, Meeting abstract suppl., abstract no. 572.1 How to Cite?
AbstractLevels of 15-F2t-isoprostane (IsoP), a specific marker of oxidative stress and a recently identified independent predictor of myocardial morbidity in patients with ischemic heart disease, are increased in the myocardium and plasma in Type 1 diabetes. The beta isoform of Protein kinase C (PKCβ) is over-expressed in the myocardium of diabetic rodents and contributes to the development of diabetic cardiomyopathy and associated complications. We postulated that selective PKCâ inhibition with ruboxistaurin would attenuate hyperglycemia-induced oxidative stress and normalize IsoP production. Control or streptozotozin-induced diabetic rats were treated (DT) or untreated (C, D) with ruboxistaurin (1 mg/kg/day) delivered by oral gavage for four weeks. Myocardial IsoP content, cardiac mass and plasma IsoP were significantly increased while there was a significant decrease in superoxide dismutase activity in D compared to C rats (all P<0.05). Ruboxistaurin treatment normalized all these changes. It is concluded that ruboxistaurin may have prevented hyperglycemia-induced oxidative stress by restoring endogenous antioxidant enzyme superoxide dismutase activity in diabetes.
DescriptionOpen Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/126868
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorLei, Sen_HK
dc.contributor.authorLiu, HMen_HK
dc.contributor.authorMao, Xen_HK
dc.contributor.authorWong, GTCen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorIrwin, MGen_HK
dc.contributor.authorXia, Zen_HK
dc.date.accessioned2010-10-31T12:53:18Z-
dc.date.available2010-10-31T12:53:18Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 2010 Annual Meeting of Experimental Biology (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24, Meeting abstract suppl., abstract no. 572.1en_HK
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/126868-
dc.descriptionOpen Access Journal-
dc.description.abstractLevels of 15-F2t-isoprostane (IsoP), a specific marker of oxidative stress and a recently identified independent predictor of myocardial morbidity in patients with ischemic heart disease, are increased in the myocardium and plasma in Type 1 diabetes. The beta isoform of Protein kinase C (PKCβ) is over-expressed in the myocardium of diabetic rodents and contributes to the development of diabetic cardiomyopathy and associated complications. We postulated that selective PKCâ inhibition with ruboxistaurin would attenuate hyperglycemia-induced oxidative stress and normalize IsoP production. Control or streptozotozin-induced diabetic rats were treated (DT) or untreated (C, D) with ruboxistaurin (1 mg/kg/day) delivered by oral gavage for four weeks. Myocardial IsoP content, cardiac mass and plasma IsoP were significantly increased while there was a significant decrease in superoxide dismutase activity in D compared to C rats (all P<0.05). Ruboxistaurin treatment normalized all these changes. It is concluded that ruboxistaurin may have prevented hyperglycemia-induced oxidative stress by restoring endogenous antioxidant enzyme superoxide dismutase activity in diabetes.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_HK
dc.subjectBiology-
dc.titlePKC β inhibitor ruboxistaurin prevents the increase of 15-F2t-isoprostane in the myocardium and plasma in Type 1 diabetic ratsen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0892-6638&volume=24, Meeting Abstract Suppl., abstract no. 572.1 &spage=&epage=&date=2010&atitle=PKC+β+inhibitor+ruboxistaurin+prevents+the+increase+of+15-F2t-isoprostane+in+the+myocardium+and+plasma+in+Type+1+diabetic+rats-
dc.identifier.emailLei, S: leishaoqing@163.comen_HK
dc.identifier.emailLiu, HM: huimin_liu2006@126.comen_HK
dc.identifier.emailWong, GTC: gordon@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailIrwin, MG: mgirwin@hku.hken_HK
dc.identifier.emailXia, Z: zhengyuan_xia@yahoo.comen_HK
dc.identifier.authorityWong, GTC=rp00523en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.identifier.authorityIrwin, MG=rp00390en_HK
dc.identifier.authorityXia, Z=rp00532en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros171204en_HK
dc.identifier.volume24en_HK
dc.identifier.issueMeeting abstract suppl.-
dc.description.otherExperimental Biology Annual Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24, Meeting abstract suppl., abstract no. 572.1-

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