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Life Sci. 2016 May 15;153:82-92. doi: 10.1016/j.lfs.2016.04.017. Epub 2016 Apr 14.

Selective inhibition of COX-2 improves cutaneous wound healing of pressure ulcers in mice through reduction of iNOS expression.

Author information

1
Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: bruna.souza@uerj.br.
2
Histocompatibility and Cryopreservation Laboratory, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
3
Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.

Abstract

AIMS:

Cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) are involved in chronic inflammation observed in chronic lesions. Nonetheless, neither study demonstrated if decreased COX-2 activation could promote the wound healing of pressure ulcers. Therefore, this study investigated the effect of the administration of celecoxib (a selective COX-2 inhibitor) in wound healing of pressure ulcers.

MATERIALS AND METHODS:

Male mice were treated daily with celecoxib until euthanasia. One day after the beginning of treatment, two cycles of ischemia-reperfusion by external application of two magnetic plates were performed in skin to induce pressure ulcer formation.

KEY FINDINGS:

Celecoxib administration reduced the protein expression of inducible nitric oxide synthase (iNOS), COX-2 and PGE2. The hydroperoxide levels, neutrophil and macrophage number, and protein elastase and matrix metalloproteinase-1 levels were reduced in celecoxib-treated group when compared to control group. Celecoxib administration increased myofibroblastic differentiation, re-epithelialization and wound contraction, and decreased the skin necrosis and angiogenesis. Celecoxib administration also stimulated the formation of a more organized and mature scar increasing collagen deposition and reducing tenascin-C expression.

SIGNIFICANCE:

Celecoxib administration improves the wound healing of pressure ulcers through decreased expression of iNOS and COX-2, which reduces wound inflammation and promotes dermal reconstruction and scar formation.

KEYWORDS:

Celecoxib; Cyclooxygenase-2; Mice; Pressure ulcer; Prostaglandin E(2)

PMID:
27091651
DOI:
10.1016/j.lfs.2016.04.017
[Indexed for MEDLINE]

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