Abstract: Pre-eclampsia is one of the most common complication in pregnancy, it can not only lead to placental abruption, maternal liver and kidney damage, premature delivery, fetal growth restriction, etc., but also is the most common cause of maternal and perinatal mortality. Because of its serious harm to mother and child health, its pathogenesis has long been a hot issue of obstetrical research. Uterine spiral artery remodeling disorders, vascular endothelial damage, genetic, immune imbalance and inflammatory responses are related to the pre-eclampsia. Among these factors, a wide range damage of vascular endothelial cells is regarded as the key pathological mechanisms in the development of pre-eclampsia. Recent studies have proved that vascular endothelial damage is mainly caused by oxidative stress and the increased level of soluble endoglin (sEng), soluble vascular endothelial growth factor receptor 1（ｓＦｌｔ－１）. However, we found that heme oxygenase-1（ＨＯ－１）, an inducible antioxidant enzyme, along with its metabolites such as carbon monoxide(CO), bilirubin can not only play an important role in normal pregnancy by maintaining placental function ,promoting the development of placenta and fetal growth, but also has significant function in suppressing the occurrence of preeclampsia by reducing oxidative stress through activating the protective signaling pathways, increasing NADPH level and by protecting endothelial vascular function through reducing endothelial injury factors such as sEng, sFlt-1, promoting endothelial protective factor such as VEGF. Therefore, we expected that HO-1 and its metabolites can bring new breakthroughs in the prevention and treatment of pre-eclampsia.

Key words: Pre-eclampsia, Heme oxygenase（Decyclizing）, Endothelial cells, Oxidative stress