Necrostatin-1, RIP1/RIP3 inhibitor, relieves transforming growth factor β-induced wound-healing process in formation of hypertrophic scars

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-beta 1 (TGF-beta 1) 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-beta 1-induced cell proliferation and promoted G0/G1 phase arrest in HSF. In addition, Nec-1 attenuated TGF-beta 1-induced cell migration and inhibited the expression of MMP2 and MMP9 in TGF-beta 1-induced HSF. Besides, Nec-1 also reduced TGF-beta 1-induced collagen production and alpha-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.