Objective:Periplocin is an active digitalis-like component from Cortex Periplocae,which has been widely used in the treatment of heart diseases in China for many years.According to the recommendations on the cardiovascular effect of periplocin from in vivo experiments,subsequent in vitro experiments are greatly needed for the global assessment of periplocin.The objective of this study is to investigate the cell proliferation effect and the mechanism of periplocin on endothelial cells.Methods:The proliferative activity of periplocin(0.4, 2,10,50,250μmol/L;6,12,24,48,72 h) was investigated by a comparison with the well-reported cardiac glycoside,ouabain,on mouse cardiac microvascular endothelial cells(CMEC).3-(4,5-dimethylthiazolyl)- 2,5-diphenyltetrazolium bromide(MTT),lactate dehydrogenase(LDH) and 5-bromo-2-deoxyuridine(BrdU) assays were used to evaluate cell proliferation and viability.Subsequently,cDNA microarray experiments were performed on periplocin-(50μmol/L) and ouabain-(50μmol/L) treated cells,and data was analyzed by ArrayTrack software.Results:Periplocin could increase cell viability to a level lower than ouabain in the MTT analysis,but decrease LDH release simultaneously.The BrdU incorporation assay showed an increase in cell proliferation with 2-50μmol/L periplocin.Genes related to protein serine/threonine kinase were the most significantly enriched in the 160 genes identified in periplocin versus the control.In the 165 genes regulated by periplocin versus ouabain,GTP-binding was the most altered term.Conclusions:The results demonstrated the proliferation action of periplocin on CMEC.Meanwhile,its lower cytotoxicity compared to ouabain provides a new insight into the treatment of heart failure. Objective: Periplocin is an active digitalis-like component from Cortex Periplocae, which has been widely used in the treatment of heart diseases in China for many years. According to the recommendations on the cardiovascular effect of periplocin from in vivo experiments, subsequent in vitro experiments these greatly needed for the global assessment of periplocin. The objective of this study is to investigate the cell proliferation effect and the mechanism of periplocin on endothelial cells. Methods: The proliferative activity of periplocin (0.4, 2, 10, 50, 250 μmol / L; 6,12,24,48,72 h) was investigated by a comparison with the well-reported cardiac glycoside, ouabain, on mouse cardiac microvascular endothelial cells (CMEC) .3- (4,5-dimethylthiazolyl) diphenyltetrazolium bromide (MTT), lactate dehydrogenase (LDH) and 5-bromo-2-deoxyuridine (BrdU) assays were used to evaluate cell proliferation and viability. cDNA microarray experiments were performed on periplocin- (50 μmol / L) and ouabain- (50 mol / L) treated cells, and data was analyzed by ArrayTrack software. Results: Periplocin could increase cell viability to a level lower than ouabain in the MTT analysis, but decrease LDH release simultaneously. The BrdU incorporation assay showed an increase in cell proliferation with 2-50 μmol / L periplocin.Genes related to protein serine / threonine kinase were the most significantly enriched in the 160 genes identified in periplocin versus the control. The 165 genes regulated by periplocin versus ouabain, GTP-binding was the most altered term. Conclusions: The results demonstrated the proliferation action of periplocin on CMEC .Meanwhile, its lower cytotoxicity compared to ouabain provide a new insight into the treatment of heart failure.