Cardamonin Shows Antifibrotic Activity in Human Keloid Fibroblasts: Study

Cardamonin demonstrated antifibrotic activity in human keloid fibroblasts by suppressing transforming growth factor β1 (TGF-β1)/Smad signaling, according to new in vitro research in the Journal of Drugs in Dermatology.

Investigators treated a human keloid fibroblast cell line (KEL FIB) with increasing concentrations of cardamonin, assessing proliferation, clonogenic growth, apoptosis, migration, and invasion using CCK-8, colony formation, flow cytometry, wound-healing, and Transwell assays. Immunofluorescence, RT-qPCR, and western blotting were used to examine myofibroblast and ECM-related markers.

Cardamonin Reduces Keloid Fibroblast Proliferation and ECM Production

Cardamonin inhibited keloid fibroblast proliferation, migration, and invasion in a dose-dependent manner, according to the results. Treatment also promoted apoptosis, accompanied by modulation of the BAX/BCL2 ratio and activation of caspase-3.

Cardamonin reduced α-SMA and vimentin expression as well as the ECM proteins collagen I, collagen III, and fibronectin. Mechanistically, treatment attenuated TGF-β1-induced phosphorylation of Smad2/3. The authors said the findings are limited to a cell-line model and do not establish the efficacy or safety of cardamonin as a keloid treatment in humans.

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

Source

Jin M, et al. Journal of Drugs in Dermatology. 2026. 25(9):857.