Muscle regeneration in dystrophic mdx mice is enhanced by isosorbide dinitrate

dc.creatorMarques, MJ
dc.creatorLuz, MAM
dc.creatorMinatel, E
dc.creatorSanto Neto, H
dc.date2005
dc.date42186
dc.date2014-11-14T07:37:05Z
dc.date2015-11-26T17:13:55Z
dc.date2014-11-14T07:37:05Z
dc.date2015-11-26T17:13:55Z
dc.date.accessioned2018-03-29T00:02:16Z
dc.date.available2018-03-29T00:02:16Z
dc.identifierNeuroscience Letters. Elsevier Ireland Ltd, v. 382, n. 3, n. 342, n. 345, 2005.
dc.identifier0304-3940
dc.identifierWOS:000230065800029
dc.identifier10.1016/j.neulet.2005.03.023
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/82086
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/82086
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/82086
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1281687
dc.descriptionActivation of muscle satellite cells, a fundamental step in the success of muscle regeneration is mediated by nitric oxide (NO). In this study, we investigated whether isosorbide dinitrate (ISD), an NO donor, could improve muscle regeneration in dystrophic mdx mice. The right tibialis anterior muscle of mdx and C57B1/10 mice was injected with bupivacaine (0.3 ml, 33 mg/kg), a myotoxic agent, to induce muscle fiber regeneration. After bupivacaine injection, mice were treated with ISD (30 mg/kg; i.p.), verapamil (a non-NO donor vasodilator, 15 mg/kg, i.p.) or saline solution (vehicle, 0.3 ml, i.p.) for 20 days. Some bupivacaine-injected mice received no pharmacological treatment (control group). Muscle regeneration was evaluated by counting the total number of muscle fibers and measuring myofiber cross-sectional area. ISD significantly improved bupivacaine-induced muscle regeneration in mdx by increasing by 20% the total number of muscle fibers compared to the other groups. Spontaneous muscle regeneration, evaluated in the contralateral non-injected muscle, was not affected. ISD treatment did not affect myofiber cross-sectional area. Verapamil and saline had no effect on muscle regeneration. These results suggested that NO derived from ISD stimulated and/or recruited satellite cells. Pharmacological treatment with ISD could be clinically useful for improving muscle regeneration in Duchenne muscular dystrophy. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
dc.description382
dc.description3
dc.description342
dc.description345
dc.languageen
dc.publisherElsevier Ireland Ltd
dc.publisherClare
dc.publisherIrlanda
dc.relationNeuroscience Letters
dc.relationNeurosci. Lett.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectDMD
dc.subjectisosorbide dinitrate
dc.subjectmuscle regeneration
dc.subjectmdx
dc.subjectnitric oxide
dc.subjectDuchenne Muscular-dystrophy
dc.subjectNitric-oxide Synthase
dc.subjectIsosorbide-5-mononitrate 60 Mg
dc.subjectSkeletal-muscle
dc.subjectSatellite Cells
dc.subjectGrowth-factor
dc.subjectL-arginine
dc.subjectRelease
dc.subjectMultitab(r)
dc.subjectTherapy
dc.titleMuscle regeneration in dystrophic mdx mice is enhanced by isosorbide dinitrate
dc.typeArtículos de revistas


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