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Updated: Jun 17, 2026
A Mouse Model of Mechanotransduction-driven, Human-like Hypertrophic Scarring
Published on: November 29, 2024
Botulinum Toxin Type A Alleviates Hypertrophic Scar Formation in a Rabbit Ear Model by Inhibiting the TGF-β1/Smad
Yue-Hua Li1,2, Xiao-Wen Li1, Lei Ren1
1Department of Geriatric General Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Background:
Postoperative hypertrophic scarring represents a prevalent clinical challenge, with current therapeutic approaches demonstrating limited efficacy. Previous studies have confirmed the scar-inhibitory properties of Botulinum toxin type A (BTA), though its precise molecular mechanisms require further elucidation. This study aims to explore the molecular pathways through which BTA attenuates hypertrophic scar formation using an established auricular cicatricial model in rabbits.
Methods:
Sixteen healthy New Zealand white rabbits underwent hypertrophic scar modeling. Post-modeling, therapeutic interventions were administered as follows: BTA (4U) was injected at the edge of the wound in the BTA group and the combined group, whereas, decorin (50 µg) was injected at the edge of the wound in the decorin group and the combined group. Decorin administration was repeated following a seven-day interval. The control group was administered an equivalent volume of normal saline. The scar height, collagen deposition and TGF-β1 expression level were measured by histological examination. Protein expression profiles were evaluated through immunoblotting techniques.
Results:
Our results revealed that hypertrophic scars were reduced in all treatment groups compared with the control group. BTA- and/or decorin-treated group had lower scar height, collagen deposition and TGF-β1 expression level at week 4 and week 8. BTA and/or decorin effectively suppressed the Smad2/3 phosphorylation cascade, inhibited MMP2 enzymatic activity, and reduced the protein expression of α-SMA and collagen I.
Conclusion:
BTA improves the appearance of scar, reduces collagen deposition, and decreases the degree of scar formation by inhibiting the TGF-β1/Smad signaling pathway in a rabbit ear model.
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