Journal of cosmetic dermatology · 2020
Botulinum toxin type A attenuates hypertrophic scar formation via the inhibition of TGF-β1/Smad and ERK pathways.
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Li Yue-Hua, Yang Jiaomei, Zheng Zhao, Hu Da-Hai, Wang Zhi-Dong
Аннотация
BACKGROUND: Hypertrophic scar is a common complication in would healing process, and how to effectively prevent and treat it has been a hot and difficult research issue. Previous studies have showed that botulinum toxin type A (BTA) has effects on the prevention and treatment of hypertrophic scar, but little is known about the specific mechanisms.
OBJECTIVE: This study aimed to explore the potential mechanisms of BTA on the inhibition of hypertrophic scar formation.
METHODS: Hypertrophic scar-derived human fibroblasts were cultured and then treated with transforming growth factor-β1 (TGF-β1) and various concentrations of BTA. Cell proliferation and viability were measured by CellTiter 96® AQueous One Solution Cell Proliferation Assay and trypan blue staining, respectively. The total amount of collagen was examined using Sirius red staining. Collagen I and Collagen III in the culture supernatant were evaluated by enzyme-linked immunosorbent assay. Reverse transcription-quantitative polymerase chain reaction and Western blot analysis were performed to detect the transcription and translation levels.
RESULTS: Our results revealed that BTA decreased the proliferation of hypertrophic scar-derived human fibroblasts. The mRNA and protein expression levels of alpha-smooth muscle actin, collagen I, and collagen III induced by TGF-β1 were inhibited by BTA in a dose-dependent manner. BTA also inhibited the phosphorylation of Smad2/3 and ERK.
CONCLUSION: BTA decreased the proliferation of fibroblasts and prevented overdeposition of ECM through the inhibition of the TGF-β1/Smad and ERK pathways. The findings of this study provide new scientific reference for the prevention and treatment of hypertrophic scar.
OBJECTIVE: This study aimed to explore the potential mechanisms of BTA on the inhibition of hypertrophic scar formation.
METHODS: Hypertrophic scar-derived human fibroblasts were cultured and then treated with transforming growth factor-β1 (TGF-β1) and various concentrations of BTA. Cell proliferation and viability were measured by CellTiter 96® AQueous One Solution Cell Proliferation Assay and trypan blue staining, respectively. The total amount of collagen was examined using Sirius red staining. Collagen I and Collagen III in the culture supernatant were evaluated by enzyme-linked immunosorbent assay. Reverse transcription-quantitative polymerase chain reaction and Western blot analysis were performed to detect the transcription and translation levels.
RESULTS: Our results revealed that BTA decreased the proliferation of hypertrophic scar-derived human fibroblasts. The mRNA and protein expression levels of alpha-smooth muscle actin, collagen I, and collagen III induced by TGF-β1 were inhibited by BTA in a dose-dependent manner. BTA also inhibited the phosphorylation of Smad2/3 and ERK.
CONCLUSION: BTA decreased the proliferation of fibroblasts and prevented overdeposition of ECM through the inhibition of the TGF-β1/Smad and ERK pathways. The findings of this study provide new scientific reference for the prevention and treatment of hypertrophic scar.