"Keloids represent a dysregulated response to cutaneous wounding that results in an excessive deposition of extracellular matrix. However, the molecular mechanisms underlying this pathologic deposition of extracellular matrix still remain to be elucidated. In this study, the effects of anti-keloid drugs (triamcinoloneⓇ, 5-FUⓇ, bleomycinⓇ, verapamilⓇ) on the expression of fibronectin and TGF-β and its receptor in keloid fibroblasts were evaluated in vitro. Human keloid fibroblasts(KFs) and normal human dermal fibroblasts(NHDFs) were isolated from earlobe keloids. Immunoprecipitation and Western blot of fibronectin, ELISA of TGF-β secretion and Western blot of TGF-β receptor were performed using the primary cultured fibroblasts treated with various drugs. TGF-β secretion was increased in keloid fibroblasts compared to NHDFs. TGF-βpromoted fibronectin synthesis in keloid fibroblasts. These results substantiate the hypothesis that the elevated levels of TGF-β play a potential role in keloid pathogenesis. 5-FU suppressed profoundly TGF-β secretion. Triamcinolone and verapamil inhibited significantly fibronectin synthesis and secretion, and also suppressed TGF-β receptor expression in keloid fibroblasts.  In conclusion, it is postulated that the combination of low dose of 5-FU and triamcinolone or verapamil may be useful in keloid treatment by the additive effect of different anti-keloid action. "