Uighur medicine abnormal savda munzip (ASMq) suppresses expression of collagen and TGF-β1 with concomitant induce Smad7 in human hypertrophic scar fibroblasts.

BACKGROUND

Hypertrophic scar (HS) is a common dermal disease, for which numerous treatments are currently available but they do not always yield excellent therapeutic results. Hence, alternative strategy are needed. Recent basic and clinic research has shown that Uighur medicine abnormal savda munzip (ASMq) has anti-hypertrophic scar properties but its molecular mechanism is unknown. The aim of this study was to explore the effect of ASMq on TGF-β/Smads signaling in fibroblasts derived from hypertrophic scar.

PURPOSE: To investigate the effect of ASMq on the TGF-β/Smads signaling pathway in hypertrophic scar fibroblasts (HSFs).

METHODS

Hypertrophic scar fibroblasts (HSFs) were isolated from human of hypertrophic scar and passaged to the 3~4 generation, which were treated with the different concentrations of ASMq. Cells treated with 5-Fu served as the positive control group. After treatment for 48 hours, expressions of Smad7, TGF-β1, type I and III collagen, were examined by immunocytochemistry, reverse transcription PCR and Western blotting, respectively.

RESULTS

ASMq markedly enhanced the expression of inhibitory Smad7, with suppression of type I and III collagen and TGF-β1. We observed that treatment of ASMq induced Smad7 to enter the cytoplasm from the nucleus of hypertrophic fibroblasts.

CONCLUSIONS

ASMq inhibits scarring probably by enhancing the expression of inhibitory Smad7, and inhibiting TGF-β1, collagen expression, and is a potential treatment for scarring.