Selective inhibition of COX-2 improves cutaneous wound healing of pressure ulcers in mice through reduction of iNOS expression.
Life Sci
; 153: 82-92, 2016 May 15.
Article
in En
| MEDLINE
| ID: mdl-27091651
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 ANDMETHODS:
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. KEYFINDINGS:
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.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Wound Healing
/
Pressure Ulcer
/
Nitric Oxide Synthase Type II
/
Cyclooxygenase 2 Inhibitors
Limits:
Animals
Language:
En
Journal:
Life Sci
Year:
2016
Document type:
Article