Low Dose Treatment of RhTGF-beta1 Restore the Wound Healing Defect in Dexamethasone-treated Rats / 체질인류학회지
Korean Journal of Physical Anthropology
;
: 207-215, 2010.
Artículo
en Coreano
| WPRIM
| ID: wpr-37918
ABSTRACT
Transforming growth factor-beta1 (TGF-beta1) has chemotactic effect to monocytes, macrophages and fibroblasts, and it stimulates those cells to produce growth factors and collagen fibers. Therefore, TGF-beta1 plays important roles in the wound healing process. The aim of this study is to evaluate the effects of recombinant human TGF-beta1 (rhTGF-beta1) on the wound healing defect in dexamethasone-treated rats. Dexamethasone (0.1 mg/kg/day) was subcutaneously injected into the eight-week-old Sprague-Dawley rats. At the third day of dexamethasone administration, full thickness wounds were made on the back of the rat. And then, rhTGF-beta1 (50 ng/wound) was intradermally injected in the vicinity of the wounds. The wounds of the normal and the negative control groups were provided with vehicle only. At 1, 3, 5, 7 and 15 days after the surgery, the wound sizes were measured and the wound tissues were obtained and analyzed. The mean wound sizes of the rhTGF-beta1 injected groups were significantly smaller than those of the negative control groups. Moreover, the histologic findings such as cellular infiltration, re-epithelialization and granulation formation and expression patterns of TGF-betas during the wound healing process were improved by administration of rhTGF-beta1. These results support that rhTGF-beta1 can restore wound healing defect due to dexamethasone administration.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Cicatrización de Heridas
/
Dexametasona
/
Monocitos
/
Factor de Crecimiento Transformador beta
/
Colágeno
/
Ratas Sprague-Dawley
/
Péptidos y Proteínas de Señalización Intercelular
/
Factor de Crecimiento Transformador beta1
/
Fibroblastos
/
Repitelización
Límite:
Animales
/
Humanos
Idioma:
Coreano
Revista:
Korean Journal of Physical Anthropology
Año:
2010
Tipo del documento:
Artículo
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