Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/35166
Title: Dual role of cyclooxygenase-2 during tissue repair induced by low level laser therapy: An intriguing issue
Authors: Ribeiro, Daniel A. [UNIFESP]
Paiotti, Ana Paula R. [UNIFESP]
Medalha, Carla C. [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Keywords: cyclooxygenase-2
tissue repair
low level laser therapy
Issue Date: 1-Aug-2012
Publisher: Informa Healthcare
Citation: Journal of Cosmetic and Laser Therapy. London: Informa Healthcare, v. 14, n. 4, p. 184-188, 2012.
Abstract: Tissue repair is an excellent example of pathophysiological model for studying the role of cyclooxygenase-2 (COX-2) on eukaryotic cells. It has been established that two COX isoforms are expressed in human tissues: constitutive or induced. COX-1 activity is constitutive, present in nearly all cell types at a constant level; COX-2 activity is normally absent from cells, and when induced, the protein levels increase and decrease in a matter of hours after a single stimulus. Thus, the purpose of this review was to describe the role of COX-2 during tissue repair induced by low level laser therapy (LLLT) in humans and experimental models. COX-2 expression has been implicated in the onset or the exacerbation of inflammation during tissue repair induced by LLLT in a number of studies, Many studies are conducted to investigate the role of COX-2 during tissue repair induced by LLLT using different experimental protocols and dosages. Therefore, this is an area that warrants investigation, since the estimation of COX-2 expression from using such important techniques in therapeutics with respect to tissue repair will be added to those already established in the literature as a way to improve health status and prevention of side effects.
URI: http://repositorio.unifesp.br/handle/11600/35166
ISSN: 1476-4172
Other Identifiers: http://dx.doi.org/10.3109/14764172.2012.685479
Appears in Collections:Em verificação - Geral

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.