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

Abstract

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