dc.creatorMarques, MJ
dc.creatorBarbin, ICC
dc.creatorTaniguti, APT
dc.creatorOggian, DS
dc.creatorFerretti, R
dc.creatorNeto, HS
dc.date2010
dc.dateJUN
dc.date2014-08-01T18:39:36Z
dc.date2015-11-26T17:06:35Z
dc.date2014-08-01T18:39:36Z
dc.date2015-11-26T17:06:35Z
dc.date.accessioned2018-03-28T23:55:03Z
dc.date.available2018-03-28T23:55:03Z
dc.identifierActa Biologica Hungarica. Akademiai Kiado Rt, v. 61, n. 2, n. 168, n. 174, 2010.
dc.identifier0236-5383
dc.identifierWOS:000278276800005
dc.identifier10.1556/ABiol.61.2010.2.5
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/81937
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/81937
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1279897
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionCardiac failure secondary to myocardial fibrosis (MF) significantly contributes to death in Duchenne muscular dystrophy (DMD), a fatal form of muscle disease. In aging, the mdx mice, an animal model of DMD, MF is similar to that observed in humans. Nitric oxide-based therapy has been proposed to retard MF in DMD and a candidate is L-arginine (L-arg). In this study we evaluated the effects of long-term therapy with L-arg in the MF of mdx mice. Mdx mice (6 months old) were treated with L-arg in drinking water. Control mdx mice received water only. After 15 months of treatment, hearts were stained with Masson's trichrome for analysis of MF and with hematoxilyn and eosin for analysis of inflammation and cardiomyocyte damage. We observed that MF was not affected (29.5+/-2.5% of MF area for control vs 31.4+/-2% for L-arginine-treated animals; P>0.05). The density of inflammatory cells was reduced (169+/-12 cells/mm(2) in control vs 102 +/- 9 cells/mm2 in L-arg-treated; P<0.05). The present study shows that long-term administration of L-arg is not effective in retarding MF in mdx dystrophinopathy.
dc.description61
dc.description2
dc.description168
dc.description174
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFAPESP [95/6110-2, 01/00570-4, 04/15526-9]
dc.descriptionCNPq [301386/07-2, 302006/09-5, 474708/06-3]
dc.languageen
dc.publisherAkademiai Kiado Rt
dc.publisherBudapest
dc.publisherHungria
dc.relationActa Biologica Hungarica
dc.relationActa Biol. Hung.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectCardiac failure
dc.subjectcardiac fibrosis
dc.subjectcardiomyopathy
dc.subjectDuchenne muscular dystrophy
dc.subjectDuchenne Muscular-dystrophy
dc.subjectNitric-oxide
dc.subjectMatrix Metalloproteinases
dc.subjectCardiac-function
dc.subjectHeart
dc.subjectCardiomyopathy
dc.subjectTherapy
dc.subjectPeroxynitrite
dc.subjectExpression
dc.subjectMouse
dc.titleMYOCARDIAL FIBROSIS IS UNALTERED BY LONG-TERM ADMINISTRATION OF L-ARGININE IN DYSTROPHIN DEFICIENT MDX MICE: A HISTOMORPHOMETRIC ANALYSIS
dc.typeArtículos de revistas


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