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Updated: Sep 4, 2025
A Mouse Model of Mechanotransduction-driven, Human-like Hypertrophic Scarring
Published on: November 29, 2024
Concentration-Dependent Inhibition of Hypertrophic Scar Formation by Botulinum Toxin Type A in a Rabbit Ear Model
Zhiguo Yang1, Yang Lv1, Zizheng Yang2
1Department of Plastic and Reconstructive Surgery, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, 230601, Anhui Province, People's Republic of China.
Background:
Hypertrophic scar (HS), as a disappointing result of wound healing, adversely affects the patient, both physically and psychologically. Botulinum toxin type A (BTXA) has been revealed to prevent and improve HS. We conducted this study to assess the effect of different BTXA concentrations on inhibiting HS in a rabbit ear model.
Methods:
Eight healthy New Zealand long-eared rabbits were included in the experiment for modeling. Four wounds of 1 cm in diameter were created on both ears, which separately received an injection of a given BTXA concentration immediately after surgery. On postoperative days 40, scar tissue was obtained and subjected to hematoxylin and eosin (HE) staining for the hypertrophic index (HI) and immunohistochemical staining for CD31, Ki67, and transforming growth factor-beta 1 (TGF-β1) expression. The HI was assessed for scar proliferation, and CD31 and Ki67 expression were used to assess the effect of BTXA on angiogenesis and fibroblast proliferation, respectively.
Results:
All rabbits healed well without infection or mortality. From the HE staining, the HI showed a significant decrease with increasing BTXA concentration (p < 0.05). BTXA also inhibited angiogenesis and TGF-β1 expression in a concentration-dependent manner, with significant differences between the groups (p < 0.05). BTXA inhibited fibroblast proliferation with increasing BTXA concentration. However, there was no significant difference between the 0.5 U/0.1 ml and 0 U/0.1 ml groups (p > 0.05).
Conclusion:
Immediate postoperative BTXA injection inhibited angiogenesis, fibroblast proliferation, and TGF-β1 expression in a concentration-dependent manner, thus suppressing HS formation in rabbit ears.
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