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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
Title | PKC β inhibitor ruboxistaurin prevents the increase of 15-F2t-isoprostane in the myocardium and plasma in Type 1 diabetic rats |
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Authors | |
Issue Date | 2010 |
Publisher | Federation 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 n. S1, abstract no. 572.1 How to Cite? |
Abstract | Levels 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. |
Persistent Identifier | http://hdl.handle.net/10722/126868 |
ISSN | 2023 Impact Factor: 4.4 2023 SCImago Journal Rankings: 1.412 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Liu, Y | en_HK |
dc.contributor.author | Lei, S | en_HK |
dc.contributor.author | Liu, HM | en_HK |
dc.contributor.author | Mao, X | en_HK |
dc.contributor.author | Wong, GTC | en_HK |
dc.contributor.author | Vanhoutte, PM | en_HK |
dc.contributor.author | Irwin, MG | en_HK |
dc.contributor.author | Xia, Z | en_HK |
dc.date.accessioned | 2010-10-31T12:53:18Z | - |
dc.date.available | 2010-10-31T12:53:18Z | - |
dc.date.issued | 2010 | en_HK |
dc.identifier.citation | The 2010 Annual Meeting of Experimental Biology (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 n. S1, abstract no. 572.1 | en_HK |
dc.identifier.issn | 0892-6638 | - |
dc.identifier.uri | http://hdl.handle.net/10722/126868 | - |
dc.description.abstract | Levels 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.language | eng | en_HK |
dc.publisher | Federation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/ | - |
dc.relation.ispartof | The FASEB Journal | en_HK |
dc.title | PKC β inhibitor ruboxistaurin prevents the increase of 15-F2t-isoprostane in the myocardium and plasma in Type 1 diabetic rats | en_HK |
dc.type | Conference_Paper | en_HK |
dc.identifier.email | Lei, S: leishaoqing@163.com | en_HK |
dc.identifier.email | Liu, HM: huimin_liu2006@126.com | en_HK |
dc.identifier.email | Wong, GTC: gordon@hku.hk | en_HK |
dc.identifier.email | Vanhoutte, PM: vanhoutt@hku.hk | en_HK |
dc.identifier.email | Irwin, MG: mgirwin@hku.hk | en_HK |
dc.identifier.email | Xia, Z: zhengyuan_xia@yahoo.com | en_HK |
dc.identifier.authority | Wong, GTC=rp00523 | en_HK |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_HK |
dc.identifier.authority | Irwin, MG=rp00390 | en_HK |
dc.identifier.authority | Xia, Z=rp00532 | en_HK |
dc.description.nature | abstract | - |
dc.identifier.doi | 10.1096/fasebj.24.1_supplement.572.1 | - |
dc.identifier.hkuros | 171204 | en_HK |
dc.identifier.volume | 24 | en_HK |
dc.identifier.issue | S1 | - |
dc.identifier.spage | abstract no. 572.1 | - |
dc.identifier.epage | abstract no. 572.1 | - |
dc.identifier.isi | WOS:000208675503642 | - |
dc.identifier.issnl | 0892-6638 | - |