Asiatic acid inhibits keloid fibroblast migration and collagen deposition via suppression of STAT3 activation

  • Burns. 2025 Jun 23;51(8):107586. doi: 10.1016/j.burns.2025.107586.
Jiaqi Wu  1 ,  Guizhen Xu  1 ,  Xinlu Zhou  1 ,  Jun Wan  1 ,  Huaiwei Liao  1 ,  Cong Li  1 ,  Yan Shi  2 ,  Huicai Wen  3
Affiliations
  • 1. Department of Plastic and Cosmetic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang 330001, China.
  • 2. Department of Plastic and Cosmetic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang 330001, China. Electronic address: [email protected].
  • 3. Department of Plastic and Cosmetic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang 330001, China. Electronic address: [email protected].
PMID: 40700781 DOI: 10.1016/j.burns.2025.107586
Abstract

Background: This study investigated the pharmacological effects of asiatic acid (AA) on keloid fibroblasts (KFs) and elucidated its therapeutic mechanisms in keloid pathogenesis.

Methods: Primary human KFs were isolated and expanded for experimental analysis. Cell migration capacity was evaluated through cell scratch assay and Boyden chamber assay. Immunofluorescence staining was performed to quantify α-smooth muscle actin (α-SMA) expression in AA-treated KFs, while Western blot assessed Collagen type I (Col-I), α-SMA, STAT3, and phosphorylated STAT3 (p-STAT3) protein levels. STAT3 activation was pharmacologically induced in KFs using Colivelin TFA (a STAT3 agonist), with subsequent evaluation of migratory behavior and protein expression profiles using parallel methodologies.

Results: AA treatment significantly inhibited the viability and migratory capacity of KFs, accompanied by downregulation of Col-I, α-SMA, and p-STAT3 expression. Pharmacological activation of STAT3 via Colivelin TFA partially rescued AA-induced suppression of KF migration and Col-I expression.

Conclusions: AA significantly modulates the migratory capacity and extracellular matrix (ECM)-related protein expression in KFs, with the STAT3 signaling pathway implicated in this regulatory mechanism. These findings indicate that the anti-fibrotic effects of AA are mediated through STAT3 signaling.

Keywords
Asiatic acid; Extracellular matrix; Keloid; STAT3 transcription factor.
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