Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9640
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dc.contributor.authorBonnet, Fabriceen
dc.contributor.authorCao, Zeminen
dc.contributor.authorCooper, Mark Een
dc.contributor.authorCox, Allison Jen
dc.contributor.authorKelly, D Jen
dc.contributor.authorGilbert, Richard Een
dc.date.accessioned2015-05-15T22:48:38Z
dc.date.available2015-05-15T22:48:38Z
dc.date.issued2003-09-01en
dc.identifier.citationDiabetes & Metabolism; 29(4 Pt 1): 386-92en
dc.identifier.govdoc14526266en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9640en
dc.description.abstractThe growth factors transforming growth factor-B (TGF-B) and epidermal growth factor (EGF) have both been implicated in the hypertrophic structural changes in the vasculature that are characteristic features of both human and experimental diabetes. Recently, tranilast (N(3,4-dimethoxycinnamoyl)anthranilic acid), a drug used in the treatment of allergic and dermatological diseases, has also been reported to inhibit transforming growth factor-B (TGF-B)-mediated collagen formation. However, its effects on vascular hypertrophy in diabetes are unknown. The present study thus sought to determine the effects of tranilast on both TGF-B and EGF expression and mast cells in mediating the trophic vascular changes in experimental diabetes.Vessel morphology, growth factors and collagen gene expression and matrix deposition were examined in the mesenteric arteries of control rats treated with or without tranilast, and streptozotocin-induced diabetic Sprague-Dawley rats treated with or without tranilast (200 mg/kg/day) during a 3-week period.Compared with control animals, diabetic rats had significantly increased vessel weight, wall: lumen ratio, ECM accumulation, gene expression of TGF-B1, EGF, and both alpha1 (I) and alpha1 (IV) collagen. Tranilast treatment did not influence plasma glucose or systemic blood pressure. However, tranilast significantly reduced mesenteric weight, wall: lumen ratio and matrix deposition and also attenuated the overexpression of TGF-B1, EGF, and both alpha1 (I) and alpha1 (IV) collagen mRNA in diabetic rats.These findings indicate that tranilast ameliorates pathological vascular changes observed in experimental diabetes in association with reduced growth factor expression independent of blood glucose or systemic blood pressure.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherBase Sequenceen
dc.subject.otherBlood Vessels.drug effects.pathologyen
dc.subject.otherCollagen.geneticsen
dc.subject.otherDNA Primersen
dc.subject.otherDiabetes Mellitus, Experimental.complicationsen
dc.subject.otherDiabetic Angiopathies.prevention & controlen
dc.subject.otherEpidermal Growth Factor.geneticsen
dc.subject.otherGene Expression Regulation.drug effectsen
dc.subject.otherGrowth Substances.genetics.metabolismen
dc.subject.otherHypertrophyen
dc.subject.otherImmunohistochemistryen
dc.subject.otherMaleen
dc.subject.otherPlatelet Aggregation Inhibitors.therapeutic useen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReverse Transcriptase Polymerase Chain Reactionen
dc.subject.otherTransforming Growth Factor beta.geneticsen
dc.subject.otherortho-Aminobenzoates.therapeutic useen
dc.titleTranilast attenuates vascular hypertrophy, matrix accumulation and growth factor overexpression in experimental diabetes.en
dc.typeJournal Articleen
dc.identifier.journaltitleDiabetes & metabolismen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin & Repatriation Medical Centre, Heidelberg West, Victoria. fab.so.bonnet@free.fren
dc.description.pages386-92en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/14526266en
dc.type.austinJournal Articleen
item.cerifentitytypePublications-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
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