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Updated: Oct 22, 2026

A Mouse Model of Mechanotransduction-driven, Human-like Hypertrophic Scarring
Published on: November 29, 2024
Effects of topical vildagliptin versus triamcinolone acetonide on experimentally induced hypertrophic scars in a
Zaynab Ali Nasser1, Farrah Rasool Jaafar2
1Department of Pharmacology, College of Medicine, Al-Nahrain University, Baghdad, Iraq. zaynab96ali@gmail.com.
Abstract:
The present study aimed to evaluate the effects of topical vildagliptin on experimentally induced hypertrophic scars (HTSs) in a rabbit model. A total of 40 healthy male albino rabbits were randomly assigned to five groups (n = 8): healthy control (CTRL), untreated induced HTS model (HTS model), vehicle-received (VEH), 0.1% triamcinolone acetonide-treated (TAC), and 3% vildagliptin-treated (VIL). On day 0, four full-thickness wounds extending to the cartilage were created on the ventral surface of each rabbit ear using an 8-mm biopsy punch. On day 30, topical treatment was initiated on the newly formed scars and continued twice daily for 21 days. Samples were collected on day 51 post-wounding. Outcome measures included molecular quantification of collagen type 1 (Col I), collagen type 3 (Col III), transforming growth factor-beta 1 (TGF-β1), interleukin 6 (IL-6), histopathological examination, and alpha-smooth muscle actin (α-SMA) immunoreactivity. Vildagliptin significantly reduced Col I, Col III, TGF-β1, and IL-6 compared with the HTS model group (p < 0.001). Histopathological analysis revealed a marked improvement in scar architecture, as evidenced by lower histopathological scores and a reduced scar elevation index. Masson's trichrome (MT) staining demonstrated a significant reduction in collagen deposition, accompanied by partial restoration of normal collagen fiber organization. Immunohistochemical analysis revealed no significant change in α-SMA immunoreactivity. This more likely reflects a potential incomplete suppression of myofibroblasts. Overall, these findings suggest that topical vildagliptin may represent a promising therapeutic approach for the treatment of HTSs.
