Journal of drugs in dermatology : JDD · 2026
Cardamonin Inhibits Keloid Fibroblast Activation and Extracellular Matrix Production Through Suppression of TGF-β1/Smad Signaling.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Jin Meijing, Jing Changzhe, Liu Hongmei, Lu Bo, Jin Zhezhu, Piao Minhao, Jin Zhehu, Yuan Xinghua
Аннотация
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.
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.