Objective：To explore the mechanism of IL-27 involved in the pathogenesis of preeclampsia（PE）. Methods：①Western blot was used to detect the expression of IL-27 and its receptor WSX-1 in placentas. ②Isolation and culture of primary human umbilical vein endothelial cells（HUVECs） were conducted，and the cells were identified by immunofluorescence. ③The primary HUVECs were treated with IL-27（50 ng/mL） at time points from 0.25 to 2 hours and analyzed for activated or tyrosine phosphorylated JAK2（p-JAK2） and STAT1（p-STAT1） proteins by Western blot. ④Cell treatments of each group were as follows：normal culture group（Con），DMSO culture group，JAK2 inhibitor AG490 culture group（AG490），IL-27 culture group，DMSO+IL-27 culture group，AG490+IL-27 culture group .The tube formation assays were used to detect the effects of IL-27 on the tube formation capacity of primary HUVECs. Results：① IL-27 and WSX-1 protein levels were both increased in the PE group compared with those of the control group（t=2.98０，P=0.02０；t=2.52０，P=0.04０）. ②Primary HUVECs were successfully isolated and cultured. ③After exposure to IL-27，JAK2/STAT1 pathway was activated in primary HUVECs. ④The migration and tube formation abilities of IL-27 group and DMSO+IL-27 group were significantly reduced（t=16.05０，P=0.00０；t=16.61０，P=0.00０；t=11.36０，P=0.00０；t=11.74０，P=0.00０）. There was no significantly difference between AG490 group and AG490+IL-27 group（t=0.420，P=0.770；t=0.290，P=0.790）. Conclusion：IL-27 may play a critical role in the pathogenesis of PE through JAK2/STAT1 pathway.