Investigating the impact of botulinum toxin type a on the migration of normal human dermal fibroblasts: An in vitro wound healing assay.

Background: Botulinum toxin A (BoNT‐A) is widely utilized in the management of hypertrophic and keloid scars. One proposed mechanism for scar prevention involves the inhibition of fibroblast migration in scars by BoNT‐A. However, the data regarding the effect of BoNT‐A on the migration of normal human dermal fibroblasts (NHDF) is limited. Objectives: The aim of this study was to investigate the inhibitory effect of different types and dilutions of BoNT‐A on the migration of NHDF. Methods: In vitro scratch wound assay, NHDF cells were cultured, incubated, and subjected to scratching using a sterile tip. Subsequently, the scratched NHDF monolayer was treated with different types of BoNT‐A, including onabotulinumtoxinA (ONA), incobotulinumtoxinA (INCO), prabotulinumtoxinA (PRABO), or letibotulinumtoxinA (LETI), at varying concentrations of 10, 20, 25, 40, 50, and 100 units/milliliter (U/mL). Additionally, abobotulinumtoxinA (ABO) was administered at concentrations of 33, 50, 66, 71, 100, 150, 300, and 500 U/mL. Normal saline solution (NSS) served as a negative control. The extent of NHDF migration was evaluated by comparing each dilution of BoNT‐A with the controls using high‐content imaging at the 48‐h time point. Furthermore, the viability of the of NHDF was assessed. Results: The concentrations of 25, 40, and 50 U/mL of ONA (p < 0.001) and 25 U/mL of LETI (p < 0.05) demonstrated significantly inhibited NHDF migration in comparison to the control group. Conversely, all dilutions of PRABO, INCO, and ABO exhibited comparable NHDF migration to that of the control group. Regarding NHDF viability, no significant decrease was observed across any of the BoNT‐A types and dilutions. Conclusion: Different types and dilutions of BoNT‐A demonstrated variable inhibitory effects on NHDF migration in vitro. The selection of BoNT‐A formulation may significantly impact the clinical outcome of scar prevention related to fibroblast migration. [ABSTRACT FROM AUTHOR]