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‐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.