DHMEQ, a novel NF-kappaB inhibitor, suppresses growth and type I collagen accumulation in keloid fibroblasts

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Background:Keloid is a benign dermal tumor characterized by proliferation of dermal fibroblasts and overproduction of extracellular matrix (ECM). Nuclear factor kappaB (NF-κB) plays an important role in regulation of inflammation, immune response and cell proliferation. Activation of the NF-κB pathway is thought to be closely linked to abnormal cell proliferation and ECM production in keloid fibroblasts. Objective:This study was set out to investigate the effects of a novel selective NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on keloid fibroblasts. Methods:Primary normal and keloid dermal fibroblasts were used for this study. NF-κB activity was assessed by DNA-binding assay and immunohistochemistry. The effect of DHMEQ was evaluated by cell viability, cell growth and type I collagen accumulation. Results:Basal NF-κB activity was constitutively elevated in keloid fibroblasts, indicating that this pathway is involved in keloid pathogenesis. DHMEQ markedly reduced cell proliferation and type I collagen accumulation in keloid fibroblasts. Conclusion:The inhibition of NF-κB by DHMEQ may be an attractive therapeutic approach for keloids.

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