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

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Citações na Scopus
101
Tipo de produção
article
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY-BLACKWELL
Autores
ASSIS, Livia
HAMBLIN, Michael R.
PARIZOTTO, Nivaldo A.
Citação
LASERS IN SURGERY AND MEDICINE, v.44, n.9, p.726-735, 2012
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background 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.
Palavras-chave
low-level laser therapy, photobiomodulation, muscle cryolesion, inflammatory mediators, nitrative stress, oxidative stress
Referências
  1. Adams V, 2002, CARDIOVASC RES, V54, P95, DOI 10.1016/S0008-6363(02)00228-6
  2. Amaral AC, 2001, LASER MED SCI, V16, P44, DOI 10.1007/PL00011336
  3. Assis L, 2012, LASERS MED SCI
  4. Baptista J, 2011, PHOTOMED LASER SURG, V29, P11, DOI 10.1089/pho.2009.2737
  5. Barnes PJ, 1997, NEW ENGL J MED, V336, P1066
  6. Beckman JS, 1996, AM J PHYSIOL-CELL PH, V271, pC1424
  7. Ben-Dov N, 1999, BBA-MOL CELL RES, V1448, P372, DOI 10.1016/S0167-4889(98)00147-5
  8. Bjordal JM, 2010, PHYS THER REV, V15, P7
  9. Buford TW, 2009, APPL PHYSIOL NUTR ME, V34, P745, DOI 10.1139/H09-067
  10. Chen ACH, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0022453
  11. Cressoni MDC, 2008, PHOTOMED LASER SURG, V26, P461, DOI 10.1089/pho.2007.2150
  12. Dourado DM, 2003, LASER SURG MED, V33, P352, DOI 10.1002/lsm.10237
  13. Douris P, 2006, PHOTOMED LASER SURG, V24, P377, DOI 10.1089/pho.2006.24.377
  14. Droge W, 2002, PHYSIOL REV, V82, P47
  15. El-Remessy AB, 2007, FASEB J, V21, P2528, DOI 10.1096/fj.06-7854com
  16. Filippin LI, 2011, INFLAMM RES, V60, P347, DOI 10.1007/s00011-010-0277-2
  17. Filippin LI, 2009, NITRIC OXIDE, V21, P157
  18. Fillipin LI, 2005, LASER SURG MED, V37, P293, DOI 10.1002/lsm.20225
  19. Hamblin MR, 2010, LASER SURG MED, V42, P447, DOI 10.1002/lsm.20959
  20. Huard J, 2002, J BONE JOINT SURG AM, V84A, P822
  21. Iyomasa DM, 2009, MICRON, V40, P413, DOI 10.1016/j.micron.2009.02.002
  22. Jarvinen TAHJ, 2005, AM J SPORT MED, V33, P745, DOI 10.1177/0363546505274714
  23. Kaminski HJ, 2001, NEUROMUSCULAR DISORD, V11, P517
  24. Kim YG, 2000, LASER SURG MED, V27, P420, DOI 10.1002/1096-9101(2000)27:5<420::AID-LSM1003>3.0.CO;2-K
  25. Kroncke KD, 2001, INT IMMUNOPHARMACOL, V1, P1407, DOI 10.1016/S1567-5769(01)00087-X
  26. Langen RCJ, 2004, FASEB J, V18, P227, DOI 10.1096/fj.03-0251com
  27. Leal ECP, 2010, J ORTHOP SPORT PHYS, V40, P524, DOI 10.2519/jospt.2010.3294
  28. Li Y, 2001, CURR OPIN ORTHOP, V12, P6
  29. Liu XG, 2009, PHOTOMED LASER SURG, V27, P863, DOI 10.1089/pho.2008.2443
  30. Lopes-Martins RAB, 2006, J APPL PHYSIOL, V101, P283, DOI 10.1152/japplphysiol.01318.2005
  31. Mesquita-Ferrari RA, 2011, LASER MED SCI, V26, P335, DOI 10.1007/s10103-010-0850-5
  32. Miyabara EH, 2006, AM J PHYSIOL-CELL PH, V290, pC1128, DOI 10.1152/ajpcell.00399.2005.
  33. Nakano J, 2009, EXP PHYSIOL, V94, P1005, DOI 10.1113/expphysiol.2009.047738
  34. Pallotta RC, 2012, LASER MED SCI, V27, P71, DOI 10.1007/s10103-011-0906-1
  35. Ramos L, 2012, PHOTOCHEM PHOTOBIOL, V88, P154, DOI 10.1111/j.1751-1097.2011.01030.x
  36. Renno ACM, 2011, PHOTOMED LASER SURG, V29, P5, DOI 10.1089/pho.2009.2715
  37. Rizzi CF, 2006, LASER SURG MED, V38, P704, DOI 10.1002/lsm.20371
  38. Servetto N, 2010, LASER SURG MED, V42, P577, DOI 10.1002/lsm.20910
  39. Shefer G, 2001, J CELL PHYSIOL, V187, P73, DOI 10.1002/1097-4652(2001)9999:9999<::AID-JCP1053>3.0.CO;2-9
  40. Shi XZ, 2006, GENE DEV, V20, P1692, DOI 10.1101/gad.1419406
  41. Silveira PCL, 2009, J PHOTOCH PHOTOBIO B, V95, P89, DOI 10.1016/j.jphotobiol.2009.01.004
  42. Tidball JG, 2005, AM J PHYSIOL-REG I, V288, pR345, DOI 10.1152/ajpregu.00454.2004
  43. van den Berg R, 2001, BRIT J NUTR, V86, pS121, DOI 10.1079/BJN2001340