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


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.


RESULTS
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.


CONCLUSIONS
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.
Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: bruna.souza@uerj.br.
Bruna
B
Romana-Souza
Histocompatibility and Cryopreservation Laboratory, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Jeanine Salles Dos
JS
Santos
Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Luana Graziella
LG
Bandeira
Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Andréa
A
Monte-Alto-Costa
D000818:Animals; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology*; D008297:Male; D051379:Mice; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors*; D003668:Pressure Ulcer / Q000503:physiopathology*; D014945:Wound Healing
D052246:Cyclooxygenase 2 Inhibitors; D052247:Nitric Oxide Synthase Type II
Celecoxib; Cyclooxygenase-2; Mice; Pressure ulcer; Prostaglandin E(2)