Yue-Hua Li1, Jiaomei Yang2, Zhao Zheng3, Da-Hai Hu3, Zhi-Dong Wang1. 1. Department of Geriatric Digestive Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. 2. Department of Epidemiology and Health Statistics, School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, China. 3. Department of Burns and Cutaneous Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Abstract
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.
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.