Doxycycline ameliorates the dystrophic phenotype of skeletal and cardiac muscles in mdx mice

Autor(es)

Pereira, Juliano Alves ^[1] ; Tiemi Taniguti, Ana Paula ^[1] ; Matsumura, Cintia ^[1] ; Marques, Maria Julia ^[1] ; Neto, Humberto Santo ^[1]

Afiliação do(s) autor(es)

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

• Tipo de documento: Artigo Científico
• Fonte: MUSCLE & NERVE; v. 46, n. 3, p. 400-406, SEP 2012.
• Citações Web of Science: 8

Resumo

Introduction: We examined whether doxycycline, an antibiotic member of the tetracycline family, improves the histopathology and muscle function in mdx mice, the experimental model of DMD. Methods: Doxycycline was administered for 36 days (starting on postnatal day 0) and for 9 months (starting at 8 months of age) in drinking water. Histopathological, biochemical (creatine kinase), and functional (forelimb muscle grip strength) parameters were evaluated in limb, diaphragm, and cardiac muscle. Results: Doxycycline significantly minimized the dystrophic phenotype of skeletal and cardiac muscles and improved forelimb muscle strength. The drug protected muscle fibers against myonecrosis and reduced inflammation. Furthermore, it slowed the progression of myocardial fibrosis. Conclusions: This study provides evidence that doxycycline may be a potential therapeutic agent for DMD. Muscle Nerve 46: 400406, 2012 (AU)

• Processo FAPESP: 08/58491-1 - Mecanismos de proteção da distrofia muscular: estudo proteômico e terapia farmacológica
• Beneficiário: Maria Julia Marques
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 08/54775-5 - Mecanismos de protecao da distrofia muscular: estudo proteomico e terapia farmacologica
• Beneficiário: Cintia Yuri Matsumura
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• 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