Background: We aimed to investigate the participation of adiponectin in preeclampsia, and to explore the pos-sible mechanism. Methods: A total of 52 patients with preeclampsia and 30 normal women with full-term pregnancy were en-rolled. Immunohistochemistry was used to detect the localization of MAPK and STAT5. RT-PCR was used to detect the expression of adiponectin mRNA in placental tissue of patients with preeclampsia and normal preg-nant women. Western blot was used to detect the expression of adiponectin protein, MAPK, p-MAPK, STAT5 and p-STAT5 in placental tissue of patients with preeclampsia and normal pregnant women. Results: p-p38 was highly expressed in placental trophoblasts of patients with preeclampsia, while p-STAT5 was less expressed. Expression level of p-p38 and p-STAT5 in patients with preeclampsia were significantly different from those in normal pregnant women (P<0. 01). Expression level of adiponectin mRNA was signifi-cantly lower in patients with preeclampsia than in normal pregnant women (P<0. 05). Level of p-p38 expression was negatively correlated with levels of adiponectin expression (r=-0. 413, P<0. 05). Expression level of p-STAT5 was positively correlated with expression level of adiponectin (r=0. 526, P<0. 01). Conclusion: Adiponectin participates in preeclampsia by regulating the biological function of placental tropho-blasts through p38 MAPK-STAT5 pathway.

Normal pregnancy has been considered as a controlled state of inflammation at an early stage of blastocyst implantation that subsequently develops systemically. Till recent past most popular hypotheses regarding status of immune system in pregnancy were dominated by the Thl and Th2 hypothesis, in which the fetus avoids maternal rejection through a bias towards T-helper (Th2) cytokine production. Recent findings have shown that predominant immune interactions in the human deciduas are between the placental trophoblast and maternal uterine natural killer (uNK) cells rather than the T cells. Thus NK cells are emerging as important players in the uterine immune response to invasive forms of placenta, as in cases of hemochorial placenta. In humans there is a lack of evidence for T-cell responses to trophoblast cells; therefore it was thought that uterine NK cells are the key factors by which the maternal immune system recognizes trophoblast cells. In this review we are trying to summarize the role of uNK cells in the maintenance of normal pregnancy in humans.

The placenta, as the indispensable intermediary organ between mother and fetus during pregnancy, assumes fetal nutrition for normal growth and development (1-3).The embryonic portion of human placenta arises from the blastocyst and is mainly composed of chorionic villi, as its functional and structural units (2, 4).