RESUMO
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-ß/Smads signaling in fibroblasts derived from hypertrophic scar. PURPOSE: To investigate the effect of ASMq on the TGF-ß/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-ß1, 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-ß1. 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-ß1, collagen expression, and is a potential treatment for scarring.
RESUMO
Background. To explore the effect of ASMq on proliferation and migration ability of the fibroblast derived from HS of donor (HSFbs) in vitro. Methods. The HSFbs were cultured from tissue specimens and passaged to the 3~4 generation, which were treated with the different concentrations of ASMq and 5-Fu from 1 to 11 days. The difference of HSFbs proliferation activity was analyzed by the CCK-8 method. The HSFbs migration ability in ASMq (0.4 mg/mL) was analyzed by the Cell Scratch method. Results. Transmission electron microscope result shows ASMq concentration significantly increases and fibroblast cell structure markedly change in the experimental group. The proliferation activity of the HSFbs was obviously weakened in ASMq groups than those of the group A (P < 0.05) at seven days. The group C (0.4 mg/mL) is better suitable than other three ASMq treatment groups. Cell Migration Assay shows that the migration ability HSFbs was significantly reduced in ASMq (0.4 mg/mL) treatment group compared with those of blank control group at both 24 h and 48 h (P < 0.05). Conclusions. These results suggest that ASMq effectively restrains the proliferation and migration ability of the HTSFbs in vitro, which can be one of the mechanisms for the prevention and treatment of HS.
RESUMO
BACKGROUND: To study the effect of abnormal savda munziq (ASMq) on TGF-ß1 and Smad7 expression in hypertrophic scar fibroblasts (HSFs) and to preliminarily assess the function of abnormal savda munziq in hypertrophic scar formation at the molecular biology level. METHODS: HSFs were cultured in vitro. RT-PCR and Western-blot were used to investigate the influence of 48-h treatment with ASMq at different concentrations (0 mg/mL, 0.1 mg/mL, 0.4 mg/mL, and 0.7 mg/mL) on TGF-ß1 and Smad7 mRNA and protein expression levels. RESULTS: After 48-h treatment with ASMq, the expression of TGF-ß1 mRNA and protein gradually decreased in HSFs as the concentration increased. In contrary, Smad7 mRNA and protein expression were positively correlated with ASMq concentration. CONCLUSIONS: ASMq reduces TGF-ß1, increases Smad7 mRNA and protein expression through regulating TGFß-1/Smad signaling pathway, inhibiting HSFs proliferation and reducing extracellular collagen deposition.
