Influence of vacuum-assisted closure technique on expression of Bcl-2 and NGF/NGFmRNA during wound healing / 中华整形外科杂志
Chinese Journal of Plastic Surgery
; (6): 139-142, 2004.
Article
en Zh
| WPRIM
| ID: wpr-327287
Biblioteca responsable:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To explore the influence of vacuum-assisted closure technique (VAC) on expression of Bcl-2 and NGF during wound healing.</p><p><b>METHODS</b>Eighty Sprague-Dawley rats were randomly divided into 4 groups with 20 rats of each. Group T was the experimental group; group C1, C2 and C3 were the control groups. In group T and group C1, capsaicin was injected subcutaneously to the back of the rats to destroy the sensory nerve. VAC was employed to the wound of the rats in group T and C2 three times a day at 80 mmHg negative pressure. In all the groups, tissue samples were taken from the wound edge and granulation at 1, 3, 6, 9 and 12 days after the injury. Immunohistochemistry and in situ hybridization were used to detect the expression of Bcl-2 and NGF/NGFmRNA in the samples.</p><p><b>RESULTS</b>In group C2 and C3, the expression of Bcl-2 and NGF/NGFmRNA was obvious, which increased gradually and reached the peak at the 9th day. In the process of wound healing, the expression Bcl-2 and NGF/NGFmRNA was higher in the group C2 than in group C3 (P < 0.05). The expression Bcl-2 and NGF/NGFmRNA in group T and C1 was lower than group C2 and C3 (P < 0.05).</p><p><b>CONCLUSION</b>The application of the vacuum-assisted closure technique during wound healing increases the expression of the apoptosic modulation related protein Bcl-2 and affects the expression of NGF/NGFmRNA, which may promote the wound healing process.</p>
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WPRIM
Asunto principal:
Vacio
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Cicatrización de Heridas
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ARN Mensajero
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Inmunohistoquímica
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Distribución Aleatoria
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Expresión Génica
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Ratas Sprague-Dawley
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Hibridación in Situ
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Proteínas Proto-Oncogénicas c-bcl-2
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Factor de Crecimiento Nervioso
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
Zh
Revista:
Chinese Journal of Plastic Surgery
Año:
2004
Tipo del documento:
Article