〔Abstract〕 Objective To study the protective effect of polydatin on lipopolysaccharide-induced injury of human umbilical vein vascular endothelial cells(HUVECs) through the protein Janus kinase 2(JAK2)/signal transducers and activators of transcription 3(STAT3) signaling pathway. Methods HUVECs were culturedin vitro,and 500 ng/ml LPS induced their injury and set as a model group; based on the model group, endothelial cells were intervened with different concentrations(10,20,and 40 μmol/L) of polydatin for 24 h, and set as polydatin lowconcentration group, polydatin medium concentration group, and polydatin high concentration group, respectively; a control group was set as another group.CCK-8,monocyte-endothelial cell adhesion, scratch and Transwell assays were used to detect cell viability, adhesion, migration and invasive ability; ELISA was used to detect interleukin-6(IL-6) and tumor necrosis factor-alpha(TNF-α) levels in the cell supernatant; Western blot was used to detect the expression of proteins related to the JAK2/STAT3 signaling pathway levels of JAK2/STAT3 signaling pathway related proteins. Results Compared with the control group, the model group showed decreased cell survival(P<0.01),increased cell adhesion, migration and invasion(P<0.001,P<0.05,P<0.01),increased levels of IL-6 and TNF-α in the cell supernatant(P<0.001),and increased levels of phosphorylation of JAK2 and STAT3 proteins in the cells(P<0.05).Compared with the model group, LPS damage to cells was attenuated after polydatin intervention, cell survival was increased in polydatin low-,medium-and high-concentration groups(P<0.05),cell adhesion, migration, and invasion decreased(P<0.05,P<0.05,P<0.001),IL-6 and TNF-α levels in cell supernatants decreased(P<0.05),and the levels of cellular JAK2 and STAT3 protein phosphorylation levels decreased(P<0.05). Conclusion Polydatin seems to reduce the inflammatory injury of human umbilical vein endothelial cells induced by LPS,reducing the secretion of inflammatory factors, and inhibiting the ability of cell adhesion, migration and invasion, which may be related to the down-regulation of JAK2/STAT3 signal pathway by polydatin.