Abstract
Background:
Basic fibroblast growth factor (bFGF) was clinically proven to accelerate acute and chronic wound healing. Accelerated wound healing may lead to improved scarring. These studies suggested a possible antiscarring effect of bFGF during wound healing. Little was known about the precise pathologic mechanisms of bFGF on scarring formation.
Aims:
The aim of this study was to investigate the effect of bFGF on hypertrophic scarring in a rabbit ear model and clarify the mechanism of bFGF on scar treatment.
Methods:
The rabbit model of hypertrophic scarring was created and received of a low- or high-dose topical treatment three times daily for 1, 2, or 3 months. Then we examined the changes in the macroscopic and histopathologic characteristics of the scars. The expression of collagen, α1β2 integrin, and matrix metalloproteinase 1 (MMP-1) was studied by applying reverse transcriptase-polymerase chain reaction, enzyme-linked immunosorbent assay, and Western blotting.
Result:
High-dose bFGF remarkably alleviated the scar in the rabbit ear model and decreased collagen type I expression. Further study revealed that bFGF remarkably enhanced MMP-1 and decreased α1β2 integrin expression.
Conclusion:
This study supports the hypothesis that bFGF exerted a net negative effect on collagen remodeling, therefore suggesting a potential antiscarring role.
Get full access to this article
View all access options for this article.
