Objective:To explore the mechanism of steroid receptor coactivator-3(SRC-3)involved in in the pathogenesis of preeclampsia(PE). Methods:Western blot was used to detect the expression of SRC-3 protein in placentas. Cell treatments of each group were as follows:normal culture group(N)

hypoxia/reoxygenation(H/R) culture group

lentivirus short hairpin RNA against SRC-3transfect group(sh SRC-3)

PI3 K inhibitor LY294002 culture group(LY294002). Western blot was used to detect the expression of SRC-3

p-Akt(Ser473)

Akt

p-m TOR(Ser2481)

m TOR protein in HUVECs. The tube formation assay was used to detect tube formation capacity of HUVECs. Results:The protein levels of SRC-3 were decreased in PE placentas than in normal placentas(t =3.501

P =0.013). In four cell groups

the expression of SRC-3(t=4.236

P=0.007;t=5.469

P=0.002;t=4.165

P=0.008)

p-Akt(Ser473)/Akt(t=5.214

P =0.002;t =5.188

P =0.002;t =7.054

P =0.000)

p-m TOR(Ser2481)/m TOR(t =4.832

P =0.003;t =5.695

P =0.001;t =5.699

P =0.001)proteins in H/R group

sh SRC-3 group and LY294002 group were lower than that in normal group. Moreover

the tube formation ability of H/R group

sh SRC-3 group and LY294002 group were reduced(t=5.268

P=0.002;t=4.648

P=0.004;t=4.087

P=0.009).Conclusion:These results suggest that SRC-3 may play a critical role in the pathogenesis of PE though PI3K/Akt/m TOR pathway.