Background Bone marrow stem cells in the teatment of ischemic heart disease is effective. Antiplatelet drugs including clopidogrel, ticlopidine and aspirin were usually used during stem cells transfer. The drugs can inhibit mesenchymal function and might be reduce stem cells therapy effection. Objective To investigate the effects of antiplatelet drugs on human mesenchymal stem cells (hMSCs) proliferation and secretion of VEGF. Methods After being cultured in vitro, hMSCs were treated with antiplatelet drugs. Cell proliferation was assessed by 3- (4, 5-dimethylthiazol- 2-yl)-2, 5-diphenyltet-razolium bromide (MTT) colorimetric assay, level of VEGF of culture medium was detected by enzyme-linked immunoadsordent assay (ELISA), and surface antigens of hMSCs were analyzed by the flow cytometry. Results OD570 values of hMSCs treated by clopidogrel or ticlopidine were higher than control group (P<0.01),while OD570 values of aspirin group were lower than control group (P<0.05). Treated by high dose clopidogrel or ticlopidine (40μmol/L), VEGF level from hMSCs was lower than that of control group (0.02μmol/L) (P<0.01), but VEGF level of low dose ticlopidine group was higher than control group (P<0.01) , and there was no significantly difference of VEGF level among aspirin group, low dose clopidogrel group and control group. Antiplatelet drugs had no obvious effect on cell surface antigens (CD34、CD105、CD106) expressed by hMSCs. Conclusions Clopidogrel and ticlopidine improve proliferation of hMSCs, but aspirin inhibits proliferation of hMSCs. High dose clopidogrel and ticlopidine suppress VEGF secretion of hMSCs, while low dose ticlopidine promote it. Antiplatelet drugs have no obvious effect on hMSCs differentiation. Background Bone marrow stem cells in the teatment of ischemic heart disease is effective. Antiplatelet drugs including clopidogrel, ticlopidine and aspirin were usually used during stem cell transfer. Objectives investigate the effects of antiplatelet drugs on human mesenchymal stem cells proliferation and secretion of VEGF. Methods After being cultured in vitro, hMSCs were treated with antiplatelet drugs. Cell proliferation was assessed by 3- (4,5-dimethylthiazol-2-yl) -2, 5-diphenyltet-razolium bromide (MTT) colorimetric assay, level of VEGF of culture medium was detected by enzyme-linked immunoadsordent assay (ELISA), and surface antigens of hMSCs were analyzed by the flow cytometry. Results OD570 values ​​of hMSCs treated by clopidogrel or ticlopidine were higher than control group (P <0.01), while OD570 values ​​of aspirin group were lower than control group (P <0.05). VEGF level of low dose ticlopidine group was higher than that of control group (P <0.01) (P <0.01), VEGF level of low dose ticlopidine group was higher than that of control group (0.02μmol / L) ), and there was no significant difference of VEGF level among aspirin group, low dose clopidogrel group and control group. Antiplatelet drugs had no obvious effect on cell surface antigens (CD34, CD105, CD106) expressed by hMSCs. Conclusions Clopidogrel and ticlopidine of hMSCs, but aspirin inhibits proliferation of hMSCs. High dose clopidogrel and ticlopidine suppress VEGF secretion of hMSCs, while low dose ticlopidine promote it. Antiplatelet drugs have no obvious effect on hMSCs differentiation.