Transformation of fibroblasts to myofibroblasts, characterized by expression of alpha-smooth muscle actin (alpha-SMA) and production of extracellular matrix (ECM) components, is a key event in connective tissue remodeling, it plays a critical role in the lung fibrosis development.Antiflammin-1 (AF-1, MQMKKVLDS) is a synthetic nonapeptide with a similar sequence to the conserved sequence of CC10 secreted by lung Clara cells.Studies suggest that it has many biological functions.Our previous studies indicated that AF-1 could inhibit the Human Bronchial Epithelial to Mesenchymal Transition (EMT) which induced by Transforming Growth Factorbetal (TGF-β1).In present study, we observed firstly whether AF-1 can alleviate TGF-β1-induced myofibroblast differentiation and ECM production.Cultured Mouse Lung Fibroblasts (NIH3T3) were stimulated with 5ng/ml TGF-β1 to induce myofibroblast differentiation and ECM production.