Triamcinolone acetonide suppressed scar formation in mice and human hypertrophic scar fibroblasts in a dose-dependent manner.

Abstract

A hypertrophic scar is a complex medical problem. The study of triamcinolone acetonide for the treatment of scars is necessary. The 7mm full-thickness skin wounds were created on the back of BALA/c mice to construct the animal scar model. The different doses of triamcinolone acetonide injection or normal saline were injected into the wound on the 15th, 30th and 45th day after the operation. The skin histopathological changes of mice were observed by Hematoxylin-Eosin (H&E) staining. The proteins and mRNA expression level of scar-biomarkers (COL1, COL3, α-SMA) in mice scar tissue were detected by western blot and qRT-PCR. Besides, the effect of triamcinolone acetonide on the proliferation, invasion, and migration of human hypertrophic scar fibroblast (hHSFs) in vitro was also explored by cck-8, transwell and wound healing assays. After triamcinolone acetonide was injected into the wound, the proportion of scar was significantly reduced, and the treatment effect was concentration-dependently. H&E staining showed that the skin histopathological of mice was improved dose-dependently after injecting the low/middle/high-dosage of triamcinolone acetonide. The proteins and mRNA expression levels of COL1, COL3, and α-SMA were reduced dose-dependently in mice scar tissue. Furthermore, triamcinolone acetonide dose-dependently suppressed the proliferation, invasion, and migration of hHSFs in vitro. Together, triamcinolone acetonide suppressed scar formation in mice and human hypertrophic scar fibroblasts in a dose-dependent manner, phenotypically and mechanistically. The research and further exploration of triamcinolone acetonide in treating scar formation may find new effective treatment methods for the scar.