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

BACKGROUND

Keloid is a benign dermal tumor characterized by proliferation of dermal fibroblasts and overproduction of extracellular matrix (ECM). Nuclear factor kappaB (NF-kappaB) plays an important role in regulation of inflammation, immune response and cell proliferation. Activation of the NF-kappaB 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-kappaB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on keloid fibroblasts.

METHODS

Primary normal and keloid dermal fibroblasts were used for this study. NF-kappaB 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-kappaB 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-kappaB by DHMEQ may be an attractive therapeutic approach for keloids.