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dc.contributor.authorAssis, Lívia
dc.contributor.authorMoretti, Ana Iochabel Soares
dc.contributor.authorAbrahão, Thalita Balsamo
dc.contributor.authorde Souza, Heraldo Possolo
dc.contributor.authorParizotto, Nivaldo Antonio
dc.contributor.authorHamblin, Michael R.
dc.date.accessioned2017-01-13T21:12:59Z
dc.date.available2017-01-13T21:12:59Z
dc.date.issued2012-08
dc.date.submitted2012-02
dc.identifier.issn0268-8921
dc.identifier.issn1435-604X
dc.identifier.urihttp://hdl.handle.net/1721.1/106488
dc.description.abstractMuscle regeneration is a complex phenomenon, involving replacement of damaged fibers by new muscle fibers. During this process, there is a tendency to form scar tissue or fibrosis by deposition of collagen that could be detrimental to muscle function. New therapies that could regulate fibrosis and favor muscle regeneration would be important for physical therapy. Low-level laser therapy (LLLT) has been studied for clinical treatment of skeletal muscle injuries and disorders, even though the molecular and cellular mechanisms have not yet been clarified. The aim of this study was to evaluate the effects of LLLT on molecular markers involved in muscle fibrosis and regeneration after cryolesion of the tibialis anterior (TA) muscle in rats. Sixty Wistar rats were randomly divided into three groups: control, injured TA muscle without LLLT, injured TA muscle treated with LLLT. The injured region was irradiated daily for four consecutive days, starting immediately after the lesion using an AlGaAs laser (808 nm, 30 mW, 180 J/cm[superscript 2]; 3.8 W/cm[superscript 2], 1.4 J). The animals were sacrificed on the fourth day after injury. LLLT significantly reduced the lesion percentage area in the injured muscle (p < 0.05), increased mRNA levels of the transcription factors MyoD and myogenin (p < 0.01) and the pro-angiogenic vascular endothelial growth factor (p < 0.01). Moreover, LLLT decreased the expression of the profibrotic transforming growth factor TGF-β mRNA (p < 0.01) and reduced type I collagen deposition (p < 0.01). These results suggest that LLLT could be an effective therapeutic approach for promoting skeletal muscle regeneration while preventing tissue fibrosis after muscle injury.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (grant R01AI050875)en_US
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superioren_US
dc.description.sponsorshipConselho Nacional de Pesquisas (Brazil)en_US
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Pauloen_US
dc.publisherSpringer-Verlagen_US
dc.relation.isversionofhttp://dx.doi.org/10.1007/s10103-012-1183-3en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourceSpringer-Verlagen_US
dc.titleLow-level laser therapy (808 nm) contributes to muscle regeneration and prevents fibrosis in rat tibialis anterior muscle after cryolesionen_US
dc.typeArticleen_US
dc.identifier.citationAssis, Lívia et al. “Low-Level Laser Therapy (808 Nm) Contributes to Muscle Regeneration and Prevents Fibrosis in Rat Tibialis Anterior Muscle after Cryolesion.” Lasers in Medical Science 28.3 (2013): 947–955.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Institute for Medical Engineering & Scienceen_US
dc.contributor.departmentHarvard University--MIT Division of Health Sciences and Technologyen_US
dc.contributor.mitauthorHamblin, Michael R
dc.relation.journalLasers in Medical Scienceen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dc.date.updated2016-08-18T15:21:06Z
dc.language.rfc3066en
dc.rights.holderSpringer-Verlag London Ltd
dspace.orderedauthorsAssis, Lívia; Moretti, Ana Iochabel Soares; Abrahão, Thalita Balsamo; de Souza, Heraldo Possolo; Hamblin, Michael R; Parizotto, Nivaldo Antonioen_US
dspace.embargo.termsNen
mit.licensePUBLISHER_POLICYen_US
mit.metadata.statusComplete


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