Background: Hepatic fibrosis is an extreme buildup of extracellular matrix (ECM) proteins like collagen in liver tissues. Imatinib was proven to have promising antifibrotic activity in experimental models through the suppression of platelet-derived growth factor and transforming growth factor. Tyrosine kinases have a principal role in hepatic stellate cells (HSCs) stimulation which finally enhances liver fibrosis. Imatinib as one of the Tyrosine kinases inhibitors family exhibits a great inhibition capacity in controlling HSC activation. On the other hand, Platelet-rich plasma (PRP) represents an autologous product that contains growth factors, immune system messengers, enzymes, and additional factors that have an important role in tissue regeneration. In this report, we studied the anti-fibrotic efficacy of PRP and Imatinib alone or in combination on ameliorating liver fibrosis in an animal model. Methods: In this study,