Ivermectin inhibits cell proliferation and the expression levels of type I collagen, α‑SMA and CCN2 in hypertrophic scar fibroblasts.

A hypertrophic scar (HPS) is characterized by abnormal cell proliferation and the overproduction of extracellular matrix. Currently, the treatment options available for this remain unsatisfactory. Innovative treatments are required to attenuate or prevent hypertrophic scarring and the present study searched for a drug capable of becoming a new preventative and therapeutic strategy. Although the underlying mechanisms have not been fully clarified; it is widely accepted that the TGF‑β1/SMAD3 signaling pathway serves an essential role in HPS formation. In the present study, a compound library consisting of clinically used drugs was screened for their inhibitory activity against the SMAD3 protein. The results indicated that ivermectin was able to suppress the phosphorylation of SMAD3. Therefore, the present study further investigated whether ivermectin exhibited antifibrotic effects on HPS fibroblasts. The results demonstrated that ivermectin inhibited the proliferation of HPS fibroblasts and significantly decreased the production of type I collagen, α‑smooth muscle actin and cellular communication network factor 2, as determined by analyzing the mRNA and protein expression levels. In conclusion, the results of the present study suggested that ivermectin may be a promising therapeutic agent for HPS.