Dietary compounds inhibit proliferation and contraction of keloid and XXXX scar-derived fibroblasts in vitro: therapeutic implication for excessive scarring.

@entity1 @entity15605 @entity1184 @entity4213 @entity3095 @entity6108 @entity3787 @entity2805 @entity40193 @entity3092 @entity13259 @entity16074 @entity11676
BACKGROUND: Keloid and @entity2805 commonly occur after injuries. Overproliferation of fibroblasts, overproduction of collagen, and contraction characterize these pathologic scars. Current treatment of excessive scars with intralesional corticosteroid injections used individually or in combination with other methods often have unsatisfactory outcome, frustrating both the @entity1 and the clinician. The phytochemical compounds are well known as potential anticancer agents. We have investigated the inhibitory effects of compounds on keloid fibroblasts (KF) and @entity1184 scar-derived fibroblasts (HSF). METHODS: Fibroblasts were cultured from nontreated earlobe keloids and burn @entity2805 . Ten compounds (three hydroxybenzoic and four @entity40193 derivatives, two @entity4213 [ @entity3092 and @entity15605 ], and turmeric @entity6108 ) were tested with fibroblasts. The inhibitory effects of compounds on fibroblasts was assessed by proliferation assays, fibroblast-populated collagen lattice (FPCL) contraction, and electron microscopy. RESULTS: The phytochemicals significantly inhibited KF and HSF proliferation in a dose- and time-dependent manner. In the hydroxybenzoic and @entity3095 groups, increasing inhibitory effects seemed to depend on increasing numbers of @entity3787 groups in their chemical structures. This phenomenon was not observed in the @entity40193 group. The phytochemicals inhibited fibroblast proliferation by inducing cell growth arrest but not apoptosis. The reversibility of growth inhibition occurred when the compounds were removed from the culture and fresh media was replaced. Slower reversibility of growth inhibition was observed in the groups treated with @entity3092 , @entity13259 , or @entity6108 . The compounds @entity3092 , @entity11676 , @entity16074 , and @entity13259 were the strongest inhibitors of FPLC contraction by HTFs. When the compounds were washed out of the lattices and replaced by fresh medium, the FPCL contraction was resumed. The resumption of FPCL contraction was slowest in the @entity3092 -treated group, indicating again the strong inhibitory effect of @entity3092 . CONCLUSION: From this in vitro study, @entity3092 seemed to have good potent effects to inhibit proliferation and contraction of excessive scar-derived fibroblasts.
