Journal of cosmetic dermatology · 2020
Necrostatin-1, RIP1/RIP3 inhibitor, relieves transforming growth factor β-induced wound-healing process in formation of hypertrophic scars.
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Lin Pei-Ting, Xue Xiao-Dong, Zhao Zhong-Dong, Lu Jun-Yang, Xie Pei-Lin
Аннотация
BACKGROUND: Hypertrophic scars (HS) are common pathologic processes emerged during wound-healing process. The receptor-interacting protein kinase (RIP) might participate in keloid formation.
AIMS: This study aimed to investigate Necrostatin-1 (Nec-1), a RIP1/RIP3 inhibitor, in the formation of hypertrophic scar.
METHODS: Human hypertrophic scar fibroblasts (HSF) were extracted from patients with hypertrophic scar. Transforming growth factor-β1 (TGF-β1) was performed to induce wound-healing process including cell proliferation (CCK-8, Flow cytometry, and Western blot), migration (Transwell assay, Western blot), collagen production (Western blot), and extracellular matrix dysfunction (Western blotting and immunofluorescence).
RESULTS: Our results reported that Nec-1 inhibited TGF-β1-induced cell proliferation and promoted G0/G1 phase arrest in HSF. In addition, Nec-1 attenuated TGF-β1-induced cell migration and inhibited the expression of MMP2 and MMP9 in TGF-β1-induced HSF. Besides, Nec-1 also reduced TGF-β1-induced collagen production and α-smooth muscle actin expression in HSF.
CONCLUSIONS: The present data in this study showed the potential role of Nec-1 as a novel treatment for HS.
AIMS: This study aimed to investigate Necrostatin-1 (Nec-1), a RIP1/RIP3 inhibitor, in the formation of hypertrophic scar.
METHODS: Human hypertrophic scar fibroblasts (HSF) were extracted from patients with hypertrophic scar. Transforming growth factor-β1 (TGF-β1) was performed to induce wound-healing process including cell proliferation (CCK-8, Flow cytometry, and Western blot), migration (Transwell assay, Western blot), collagen production (Western blot), and extracellular matrix dysfunction (Western blotting and immunofluorescence).
RESULTS: Our results reported that Nec-1 inhibited TGF-β1-induced cell proliferation and promoted G0/G1 phase arrest in HSF. In addition, Nec-1 attenuated TGF-β1-induced cell migration and inhibited the expression of MMP2 and MMP9 in TGF-β1-induced HSF. Besides, Nec-1 also reduced TGF-β1-induced collagen production and α-smooth muscle actin expression in HSF.
CONCLUSIONS: The present data in this study showed the potential role of Nec-1 as a novel treatment for HS.