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Background and objective—Cardiac fibrosis is one of the largest groups of cardiac diseases for which there are very few effective therapies.Our previous study demonstrated the beneficial effects of EETs administration on different models of cardiac injury.In the present study, we sought to investigate the molecular mechanisms underlying the beneficial effects of EETs on cardiac fibrosis.The effects and mechanism of 11,12-EET on collagen metabolism in cardiac myocytes and cardiac myocytes-cardiac fibroblasts co-culture system were investigated by detecting the MMP1, TIMP1, collagen Ⅰ, p-smad3 and PPAR-γ/ROS/NF-κB-P65 signaling pathway.