Objective：To evaluate the different expressions of GPR30 in placenta tissues，and their relationship with the pathogenesis of preeclampsia. Methods：Twenty cases of preeclampsia and 19 cases of normal maternal placental tissues were collected in the First Affiliated Hospital of Chongqing Medical University from January 2012 to May 2014. Immunohistochemistry was used to detect the expression of GPR30 in the placental tissues. Human umbilical vein endothelial cells（HUVECs） were used as a cell model of preeclampsia. Immunofluorescence and Western blot were used to detect the expression of GPR30 protein in HUVECs. Flow cytometry was used to detect the apoptosis of HUVECs. In vitro tube formation assay was used to detect capability of the tube formation of HUVECs and migration assay was used to detect the migration ability of HUVECs. Results：The expression of GPR30 in placental vascular endothelial cells was lower in the preeclamptic placentas than in normo-tensive controls. The expression of GPR30 protein was reduced in HUVEC after hypoxia/reoxygenation（H/R） treatment. The apoptosis of HUVECs was increased with the treatment of inhibitor of GPR30-G15. The GPR30 agonist-G1and 17β-estradiol（E2） exerted protective effects on H/R-exposed HUVECs by pro－tecting the capabilities of the tube formation and migration；this effect was abolished by G15. Conclusion：Declined expression of GPR30 may play an important role in placental endothelial dysfunction in preeclampsia.