Abstract: Objective:To explore the effect of serum from rats with rheumatic heart disease(RHD)on endothelial-mesenchymal transition(EndMT)of endothelial cells.Methods:Human umbilical vein endothelial cells(HUVECs) were first interfered with recombinant human transforming growth factor-β1(TGF-β1)to observe the occurrence of EndMT, and were divided into blank and TGF-β1 groups; HUVECs were then interfered with serum from rats and TGF-β typeⅠreceptor(TGF-β RⅠ)inhibitor SB431542, and were divided into control, RHD and RHD+SB431542 groups.The cell counting kit-8 (CCK-8) was used to measure cell proliferation ability, the wound-healing assay was used to measure cell migration ability, and real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and western blotting were performed to observe the occurrence of EndMT in cells mainly by detecting the endothelial cell marker molecule VE-cadherin and the mesenchymal cell marker molecule α-smooth muscle actin(α-SMA).Results:Compared with the control group, the RHD group had a significant increase in cell proliferation and migration ability(P< 0.05), a decreased expression of VE-cadherin protein and an elevated expression of α-SMA protein(P< 0.05), indicating the occurrence of EndMT.Compared with the RHD group, the RHD +SB431542 group had a significant reduction in cell proliferation and migration ability (P< 0.05), andthe expression of VE-cadherin protein was elevated, while the expression of α-SMA protein was reduced (P< 0.05), indicating that EndMT was significantly inhibited.Conclusion:Serum from rats with RHD highly expressing TGF-β1 can induce EndMT in HUVECs and is inhibited by SB431542, suggesting that TGF-β1 plays an important role in promoting EndMT in serum of RHD rats.