BML-111 suppresses TGF-β1-induced lung fibroblast activation in�vitro and decreases experimental pulmonary fibrosis in�vivo

Pulmonary fibrosis is an aggressive end‑stage disease. Transforming growth factor‑β1 (TGF‑β1) mediates lung fibroblast activation and is essential for the progress of pulmonary fibrosis. BML‑111, a lipoxinA4 (LXA4) receptor (ALX) agonist, has been reported to possess anti‑fibrotic properties. The present study aimed to elucidate whether BML‑111 inhibits TGF‑β1‑induced mouse embryo lung fibroblast (NIH3T3 cell line) activation in vitro and bleomycin...