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Article: Downregulation of NADPH oxidase, antioxidant enzymes, and inflammatory markers in the heart of streptozotocin-induced diabetic rats by N-acetyl-L-cysteine

TitleDownregulation of NADPH oxidase, antioxidant enzymes, and inflammatory markers in the heart of streptozotocin-induced diabetic rats by N-acetyl-L-cysteine
Authors
KeywordsNicotinamide adenine dinucleotide phosphate oxidase
Oxidative stress
Streptozotocin-induced diabetes
Issue Date2007
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2007, v. 292 n. 4, p. H1728-H1736 How to Cite?
AbstractWe investigated the effect of N-acetyl-L-cysteine (NAC) on the expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, antioxidant enzymes, and inflammatory markers in diabetic rat hearts. Metabolic parameters, free 15-F2t-isoprostane level, protein expression of NADPH oxidase, superoxide dismutase (SOD), heme oxygenase (HO-1), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2) were analyzed in control and streptozotocin-induced diabetic rats treated with or without NAC in drinking water for 8 wk. The cardiac protein expression of p67phox and p22phox was increased in diabetic rats, accompanied by increased NADPH-dependent superoxide production. As a compensatory response to the increased NADPH oxidase, the protein expression of Cu-Zn-SOD and HO-1 and the total SOD activity were also increased in diabetic rat hearts. Consequently, cardiac free 15-F 2t-isoprostane, an index of oxidative stress, was increased in diabetic rats, indicating that the production of reactive oxygen species becomes excessive in diabetic rat hearts. Cardiac inflammatory markers IL-6 and COX-2 were also increased in diabetic rats. NAC treatment prevented the increased expression of p22phox and translocation of p67phox to the membrane in diabetic rat hearts. Subsequently, the levels of cardiac free 15-F2t-isoprostane, HO-1, Cu-Zn-SOD, total SOD, IL-6, and COX-2 in diabetic rats were decreased by NAC. Consequently, cardiac hypertrophy was attenuated in diabetic rats treated with NAC. The protective effects of NAC on diabetic rat hearts may be attributable to its protection of hearts against oxidative damage induced by the increased NADPH oxidase and to its reduction in cardiac inflammatory mediators IL-6 and COX-2. Copyright © 2007 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/147242
ISSN
2023 Impact Factor: 4.1
2023 SCImago Journal Rankings: 1.452
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGuo, Zen_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorJiang, Jen_US
dc.contributor.authorMcneill, JHen_US
dc.date.accessioned2012-05-29T06:00:59Z-
dc.date.available2012-05-29T06:00:59Z-
dc.date.issued2007en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2007, v. 292 n. 4, p. H1728-H1736en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/147242-
dc.description.abstractWe investigated the effect of N-acetyl-L-cysteine (NAC) on the expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, antioxidant enzymes, and inflammatory markers in diabetic rat hearts. Metabolic parameters, free 15-F2t-isoprostane level, protein expression of NADPH oxidase, superoxide dismutase (SOD), heme oxygenase (HO-1), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2) were analyzed in control and streptozotocin-induced diabetic rats treated with or without NAC in drinking water for 8 wk. The cardiac protein expression of p67phox and p22phox was increased in diabetic rats, accompanied by increased NADPH-dependent superoxide production. As a compensatory response to the increased NADPH oxidase, the protein expression of Cu-Zn-SOD and HO-1 and the total SOD activity were also increased in diabetic rat hearts. Consequently, cardiac free 15-F 2t-isoprostane, an index of oxidative stress, was increased in diabetic rats, indicating that the production of reactive oxygen species becomes excessive in diabetic rat hearts. Cardiac inflammatory markers IL-6 and COX-2 were also increased in diabetic rats. NAC treatment prevented the increased expression of p22phox and translocation of p67phox to the membrane in diabetic rat hearts. Subsequently, the levels of cardiac free 15-F2t-isoprostane, HO-1, Cu-Zn-SOD, total SOD, IL-6, and COX-2 in diabetic rats were decreased by NAC. Consequently, cardiac hypertrophy was attenuated in diabetic rats treated with NAC. The protective effects of NAC on diabetic rat hearts may be attributable to its protection of hearts against oxidative damage induced by the increased NADPH oxidase and to its reduction in cardiac inflammatory mediators IL-6 and COX-2. Copyright © 2007 the American Physiological Society.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subjectNicotinamide adenine dinucleotide phosphate oxidase-
dc.subjectOxidative stress-
dc.subjectStreptozotocin-induced diabetes-
dc.subject.meshAcetylcysteine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Markers - Metabolismen_US
dc.subject.meshBlood Glucoseen_US
dc.subject.meshCyclooxygenase 2 - Metabolismen_US
dc.subject.meshDiabetes Mellitus, Experimental - Immunology - Metabolismen_US
dc.subject.meshDiastole - Drug Effects - Physiologyen_US
dc.subject.meshDinoprost - Analogs & Derivatives - Metabolismen_US
dc.subject.meshDown-Regulation - Drug Effects - Physiologyen_US
dc.subject.meshFree Radical Scavengers - Pharmacologyen_US
dc.subject.meshHeart Ventricles - Enzymology - Immunology - Pathologyen_US
dc.subject.meshHeme Oxygenase (Decyclizing) - Metabolismen_US
dc.subject.meshInsulin - Blooden_US
dc.subject.meshInterleukin-6 - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardium - Enzymology - Immunology - Pathologyen_US
dc.subject.meshNadph Oxidase - Metabolismen_US
dc.subject.meshOrgan Sizeen_US
dc.subject.meshOxidative Stress - Drug Effects - Physiologyen_US
dc.subject.meshPhosphoproteins - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshSuperoxide Dismutase - Metabolismen_US
dc.titleDownregulation of NADPH oxidase, antioxidant enzymes, and inflammatory markers in the heart of streptozotocin-induced diabetic rats by N-acetyl-L-cysteineen_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1152/ajpheart.01328.2005en_US
dc.identifier.pmid17122189en_US
dc.identifier.scopuseid_2-s2.0-34147095113en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34147095113&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume292en_US
dc.identifier.issue4en_US
dc.identifier.spageH1728en_US
dc.identifier.epageH1736en_US
dc.identifier.isiWOS:000245588300013-
dc.publisher.placeUnited Statesen_US
dc.identifier.citeulike1622125-
dc.identifier.issnl0363-6135-

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