Low-level laser therapy (808 nm) reduces inflammatory response and oxidative stress in rat tibialis anterior muscle after cryolesion

dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorASSIS, Livia
dc.contributor.authorMORETTI, Ana I. S.
dc.contributor.authorABRAHAO, Thalita B.
dc.contributor.authorCURY, Vivian
dc.contributor.authorSOUZA, Heraldo P.
dc.contributor.authorHAMBLIN, Michael R.
dc.contributor.authorPARIZOTTO, Nivaldo A.
dc.date.accessioned2013-07-30T14:41:53Z
dc.date.available2013-07-30T14:41:53Z
dc.date.issued2012
dc.description.abstractBackground and Objective Muscle regeneration is a complex phenomenon, involving coordinated activation of several cellular responses. During this process, oxidative stress and consequent tissue damage occur with a severity that may depend on the intensity and duration of the inflammatory response. Among the therapeutic approaches to attenuate inflammation and increase tissue repair, low-level laser therapy (LLLT) may be a safe and effective clinical procedure. The aim of this study was to evaluate the effects of LLLT on oxidative/nitrative stress and inflammatory mediators produced during a cryolesion of the tibialis anterior (TA) muscle in rats. Material and Methods Sixty Wistar rats were randomly divided into three groups (n?=?20): control (BC), injured TA muscle without LLLT (IC), injured TA muscle submitted to LLLT (IRI). The injured region was irradiated daily for 4 consecutive days, starting immediately after the lesion using a AlGaAs laser (continuous wave, 808?nm, tip area of 0.00785?cm2, power 30?mW, application time 47?seconds, fluence 180?J/cm2; 3.8?mW/cm2; and total energy 1.4?J). The animals were sacrificed on the fourth day after injury. Results LLLT reduced oxidative and nitrative stress in injured muscle, decreased lipid peroxidation, nitrotyrosine formation and NO production, probably due to reduction in iNOS protein expression. Moreover, LLLT increased SOD gene expression, and decreased the inflammatory response as measured by gene expression of NF-k beta and COX-2 and by TNF-a and IL-1 beta concentration. Conclusion These results suggest that LLLT could be an effective therapeutic approach to modulate oxidative and nitrative stress and to reduce inflammation in injured muscle. Lasers Surg. Med. 44: 726735, 2012. (c) 2012 Wiley Periodicals, Inc.
dc.description.indexMEDLINE
dc.description.sponsorshipNational Institutes of Health (NIH) [R01AI050875]
dc.description.sponsorshipEmergency Medicine Division [FMUSP-HC/LIM-51]
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2006/01096-8, 2009/01990-9]
dc.description.sponsorshipConselho Nacional de Desenvolvimento Cientifico (CNPq) [473537/2008-7, 151747/2007-5]
dc.description.sponsorshipCAPES
dc.description.sponsorshipCNPq
dc.description.sponsorshipFAPESP
dc.identifier.citationLASERS IN SURGERY AND MEDICINE, v.44, n.9, p.726-735, 2012
dc.identifier.doi10.1002/lsm.22077
dc.identifier.issn0196-8092
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/482
dc.language.isoeng
dc.publisherWILEY-BLACKWELL
dc.relation.ispartofLasers in Surgery and Medicine
dc.rightsrestrictedAccess
dc.rights.holderCopyright WILEY-BLACKWELL
dc.subjectlow-level laser therapy
dc.subjectphotobiomodulation
dc.subjectmuscle cryolesion
dc.subjectinflammatory mediators
dc.subjectnitrative stress
dc.subjectoxidative stress
dc.subject.othernf-kappa-b
dc.subject.otherskeletal-muscle
dc.subject.othernitric-oxide
dc.subject.othertranscription factor
dc.subject.otherin-vitro
dc.subject.otherirradiation
dc.subject.otherinjury
dc.subject.otherregeneration
dc.subject.otherexpression
dc.subject.otherrepair
dc.subject.wosSurgery
dc.titleLow-level laser therapy (808 nm) reduces inflammatory response and oxidative stress in rat tibialis anterior muscle after cryolesion
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.affiliation.countryEstados Unidos
hcfmusp.affiliation.countryisous
hcfmusp.author.externalASSIS, Livia:Univ Sao Paulo, Dept Phisiotherapy, Lab Electrothermophototherapy, Sao Carlos, SP, Brazil
hcfmusp.author.externalHAMBLIN, Michael R.:Massachusetts Gen Hosp, Wellman Labs Photomed, Boston, MA 02114 USA; Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA; Harvard MIT Div Hlth Sci & Technol, Cambridge, MA USA
hcfmusp.author.externalPARIZOTTO, Nivaldo A.:Univ Sao Paulo, Dept Phisiotherapy, Lab Electrothermophototherapy, Sao Carlos, SP, Brazil
hcfmusp.citation.scopus101
hcfmusp.contributor.author-fmusphcANA IOCHABEL SOARES MORETTI
hcfmusp.contributor.author-fmusphcTHALITA BALSAMO ABRAHAO
hcfmusp.contributor.author-fmusphcVIVIAN CURY
hcfmusp.contributor.author-fmusphcHERALDO POSSOLO DE SOUZA
hcfmusp.description.beginpage726
hcfmusp.description.endpage735
hcfmusp.description.issue9
hcfmusp.description.volume44
hcfmusp.lim.ref2012
hcfmusp.origemWOS
hcfmusp.origem.pubmed23001637
hcfmusp.origem.scopus2-s2.0-84867965847
hcfmusp.origem.wosWOS:000310239400005
hcfmusp.publisher.cityHOBOKEN
hcfmusp.publisher.countryUSA
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hcfmusp.remissive.sponsorshipCAPES
hcfmusp.remissive.sponsorshipCNPq
hcfmusp.remissive.sponsorshipFAPESP
hcfmusp.remissive.sponsorshipFMUSP-HC
hcfmusp.remissive.sponsorshipNIH
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hcfmusp.remissive.sponsorshipCNPq
hcfmusp.remissive.sponsorshipFAPESP
hcfmusp.remissive.sponsorshipFMUSP-HC
hcfmusp.remissive.sponsorshipNIH
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