Cardamonin Inhibits Keloid Fibroblast Activation and Extracellular Matrix Production Through Suppression of TGF-β1/Smad Signaling.

BACKGROUND

Keloids are pathological scars characterized by persistent fibroblast activation and excessive extracellular matrix (ECM) deposition. Cardamonin (CARD), a natural chalcone compound, has demonstrated anti-fibrotic effects; however, its role in keloid-associated fibrosis remains unclear. This study aimed to investigate the effects of CARD on human keloid fibroblasts (KFs) and the underlying molecular mechanisms.

METHODS

A human keloid fibroblast cell line (KEL FIB) was treated with increasing concentrations of CARD. Cell proliferation, clonogenic growth, apoptosis, migration, and invasion were assessed using CCK-8, colony formation, flow cytometry, wound healing, and Transwell assays. Myofibroblast markers and ECM-related proteins were analyzed by immunofluorescence, RT-qPCR, and western blotting. TGF-β1/Smad signaling was evaluated by assessing Smad2/3 phosphorylation.

RESULTS

CARD inhibited KF proliferation, migration, and invasion in a dose-dependent manner and promoted apoptosis through modulation of the BAX/BCL2 ratio and activation of Caspase-3. CARD reduced α-SMA and vimentin expression and decreased collagen I, collagen III, and fibronectin expression. CARD also attenuated TGF-β1-induced Smad2/3 phosphorylation.

CONCLUSION

Cardamonin exerts anti-fibrotic effects in human keloid fibroblasts by suppressing the TGF-β1/Smad signaling pathway, suggesting its potential as a pharmacological candidate for the treatment of keloids.