Objective To explore the role of vascular endothelial growth factor imbalance and abnormal complement immune activation in decidua and placenta formation during early pregnancy, and to clarify its relationship with preeclampsia. Methods Inbred BPH-5 mice were selected as preeclampsia model animals, and C57 mice were selected as control animals. The day of pregnancy was defined as day E0. 5 d. Tissues from uterine implantation sites were collected on day E5. 5 d and E7. 5 d, and placental tissues were collected from pregnant rats on day E10. 5 d. The following complement components were detected in the uterus and placenta by real-time quantitative PCR, immunohistochemistry, immunofluorescence and western blots: C3, C9, C1qa, and CfB. Additionally the expression of the following vascular endothelial growth factor (VEGF) family members was detected: VEGF, VEGFR1, VEGFR2, and sFlt-1. Results The expression of specific complement components in the uterus of BPH-5 mice was significantly increased on day E7. 5 d, during the peak period of decidualization, and the deposition of C3 and C9 was detected in the trophoblast giant cell layer of the placenta on day E10. 5 d, in the second trimester of pregnancy. On day E5. 5 d after implantation, VEGFa mRNA was significantly up-regulated, VEGFR1 and VEGFR2 mRNA levels were down-regulated, and the expression of VEGF protein was significantly increased in pregnant BPH-5 mice. The histopathological examination result showed that the decidual ratio of BPH-5 mice was significantly decreased on day E7. 5 d, and decidual angiogenesis was significantly inhibited after implantation. Conclusions In the pathogenesis of preeclampsia, the imbalance of VEGF occurs earlier than the increase in complement components at the maternal-fetal interface, and this change in maternal pregnancy precedes the occurrence of the placenta, which promotes the progression of maternal preeclampsia.