Tectochrysin suppresses the profibrotic phenotype of human keloid fibroblasts and is associated with reduced nuclear p65 accumulation.

INTRODUCTION

Keloids are fibroproliferative scars characterized by persistent fibroblast activation and excessive extracellular matrix deposition. Tectochrysin is a natural flavone with anti-inflammatory and anti-oxidative activities, but its effects on keloid fibroblasts remain unclear.

MATERIAL AND

METHODS

Human keloid fibroblasts (HKFs) and human skin fibroblasts (HSFs) were exposed to tectochrysin. Cell viability was assessed by CCK-8. HKF apoptosis, intracellular reactive oxygen species (ROS), wound closure, vimentin immunofluorescence, profibrotic protein expression, and nuclear/cytoplasmic p65 distribution were evaluated. TGF-β1-stimulated HSFs were used as a controllable profibrotic activation model.

RESULTS

Tectochrysin preferentially decreased HKF viability at 5 and 10 μg/mL while exerting weaker effects on HSFs, and significantly increased HKF apoptosis. It reduced intracellular ROS, delayed wound closure, altered vimentin-positive cytoskeletal organization in adherent HKFs, and decreased α-smooth-muscle-actin, collagen I, and fibronectin expression in HKFs. Tectochrysin also attenuated TGF-β1-induced upregulation of these markers in HSFs. Nuclear p65 abundance was reduced, whereas cytoplasmic p65 changed only modestly.

CONCLUSIONS

Tectochrysin suppresses the profibrotic phenotype of keloid fibroblasts and is associated with reduced nuclear p65 accumulation, supporting further evaluation as a candidate anti-keloid agent.