Iguratimod inhibits skin fibrosis by regulating TGF‐β1/Smad signalling pathway in systemic sclerosis

Background Iguratimod (T‐614), exerting a powerful anti‐inflammatory ability, has therapeutic efficacy in multiple autoimmune diseases. However, the effect of T‐614 on systemic sclerosis (SSc) is unclear. Here, we investigate the effect and molecular mechanism of T‐614 in experimental SSc models. Methods In vitro, cultured dermal fibroblasts from four SSc patients were subjected to different doses of T‐614 in the presence or absence of TGF‐β1 stimulation. Cell proliferation, apoptosis and migration were determined by CCK‐8, flow cytometry and transwell assay, respectively. Fibrosis markers and smad signalling pathway‐related proteins were detected by immunoblotting and immunofluorescence. In vivo, a bleomycin‐induced SSc mouse model was used to evaluate the effect of T‐614 on skin fibrosis. Pathological changes in skin tissues were evaluated by HE, Masson staining and immunohistochemistry. Results In the study, we found T‐614 inhibited TGF‐β1‐induced cell proliferation, migration and promoted apoptosis in a dose‐dependent manner (all p