Folia histochemica et cytobiologica · 2026
Tectochrysin suppresses the profibrotic phenotype of human keloid fibroblasts and is associated with reduced nuclear p65 accumulation.
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Ma Lin, Zheng Wei, Song Weibo, Ma Aijing, Zhang Qianqian, Gao Lei, Wang Hongyu
Аннотация
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.
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.