MYOCARDIAL FIBROSIS IS UNALTERED BY LONG-TERM ADMINISTRATION OF L-ARGININE IN DYSTROPHIN DEFICIENT MDX MICE: A HISTOMORPHOMETRIC ANALYSIS

Autor(es)

Marques, Maria Julia ^[1] ; Chagas Barbin, Isabel Cristina ^[1] ; Tiemi Taniguti, Ana Paula ^[1] ; Oggian, Daniela Silva ^[1] ; Ferretti, R. ^[1] ; Santo Neto, H. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Estadual Campinas, UNICAMP, Dept Anat, Inst Biol Celular Fisiol & Biofis, BR-13083970 Campinas, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: ACTA BIOLOGICA HUNGARICA; v. 61, n. 2, p. 168-174, JUN 2010.
• Citações Web of Science: 4

Resumo

Cardiac 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. (AU)

• Processo FAPESP: 01/00570-4 - Distribuição do peptídeo relacionado ao gene da calcitonina e das células de Schwann terminais, na junção neuromuscular de animais distróficos da linhagem Mdx
• Beneficiário: Maria Julia Marques
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 04/15526-9 - Proteínas reguladoras do cálcio e proteção à mionecrose na distrofia muscular de Duchenne
• Beneficiário: Maria Julia Marques
• Modalidade de apoio: Auxílio à Pesquisa - Regular