| Background:Preeclampsia is one of the serious complications during pregnancy, with the main clinical manifestations hypertension and proteiunira in the second half of pregnancy, which fades quickly after delivery. The incidence rate is 7% to 10%. It’s a serious threat to life of the mother and child health. Although the success rate of treatment of preeclampsia improves continually, its pathogenesis remains unclear. The endothelial cell dysfunction is believed as the basis of the incidence of preeclampsia widely. Pregnancy is a mild inflammatory reaction, while excessive inflammatory response damage vascular endothelial cells, leading increased vascular permeability, blood concentration, hypercoagulable in preeclampsia patients. A series of symptoms of mother are caused by the abnormal behavior of vascular endothelial cells.Human endothelial cell-specific molecule 1 (Endocan, also called ESM-1), is secreted by the endothelial cells, which is a soluble proteoglycan molecules with the weight of 50kDa. The study found that ESM-1 has a very wide range of biological activity in inflammation, angiogenesis, and also closely related to the occurrence and development of tumor. It is considered as a new marker of endothelial cell activation. It expresses more in normal human tissues than in lung and kidney tissue, but the expression level is relatively low.The Endocan level significantly increased in acute and severe inflammation, nascent tumor blood vessels.Recent reports revealed that the level of serum Endocan was significantly higher in untreated patients with essential hypertension compared with normal control group, indicating that Endocan level significantly increased when inflammation, cancer and other serious diseases happened in human body. More and more evidence show that, Endocan is a new markers of inflammation and endothelial dysfunction, therefore it plays a role in physiological or pathological in endothelium-dependent disease. In addition, Endocan is regulated by inflammatory cytokines. The tumor necrosis factor (TNF-a), interleukin (IL-1β), VEGF positively regulate the level, while interferon (y) negatively regulate it, all of which increase in preeclampsia patients serum.Normal pregnancy is a mild inflammatory reaction, while excessive inflammation and endothelial dysfunction is one of the key aspects of preeclampsia. Endocan is a new marker of endothelial cell activity, and is associated with endothelium-dependent pathological disorders, the concentration of which rise in patients with systemic inflammatory diseases. Accordingly, we speculate that blood Endocan level may vary in normal pregnancy and/or in patients with pre-eclampsia. In order to verify the above assumptions, we determined Endocan serum concentrations in non-pregnant women, normal pregnant women and patients with preeclampsia, also to explore changes of Endocan levels in normal pregnant women and in patients with preeclampsia.Objectives:To delineate the changes of maternal endocan in normal pregnancy and preeclampsia and to explore its possible role in the pathogenesis of preeclampsiaMethods:Blood samples were taken from 42 non-pregnant women,43 normal pregnant women at third trimester, and 41 preeclamptic women. Serum endocan levels were determined with enzyme-linked immuneabsorbent assay and compared among the groups.Results:There were no significant differences in serum endocan among non-pregnant women, normal pregnant women and women with preeclampsia (P=0.137) and there was no significant difference in serum endocan between women with mild and severe preeclampsia (Z=0.368,P=0.713).Conclusions:Serum endocan did not change in pregnancy and preeclampsia, indicating endocan may not be involved in the pathogenesis of preeclampsia. |