The Relationship Between Placental Thromboxane Receptor Pathway And The Pathogenesis Of Preeclampsia

Objective:1. To evaluate the difference between preeclampsia group and normal pregnancygroup in age, the weeks of terminating pregnancy, maternal blood pressure, neonatalbirth weight, fetal intrauterine growth restriction.2. To evaluate the expression of thromboxane synthase (TXS), thromboxane A2(TXA2), thromboxane receptor (TPr) and non-phagocytic cell oxidase1(NOX1) inplacenta during preeclampsia. Moreover, to research the relationship between themand the pathogenesis of preeclampsia.3. To evaluate the relationship between TXA2in preeclampsia placenta and neonatalbirth weight.4. To evaluate the relationship between TPr pathway in preeclampsia placenta and theexpression of NOX1.Methods: to collect36preeclampsia patients and34normal pregnancy1. the expression and location of TXS、TPr、NOX1were analysed withimmunohistochemistry.2. the expression of TXS、TPr、NOX1mRNA were analysed with Real-Timepolymerase chain reaction (Real-Time PCR).3. Because TXB2is stable metabolite of TXA2, the expression of TXB2in placentawas analysed with Enzyme-Linked Immuno Sorbent Assay (ELISA).Results:1. Two groups of pregnant women clinical data analysed showed that it’s nostatistically significant difference in age (P>0.05), but it has statistically significantdifferences in the weeks of terminating pregnancy, Systolic blood pressure, diastolicblood pressure, Mean arterial pressure, neonatal birth weight and fetal intrauterinegrowth restriction.2. Immunohistochemistry showed that 2.1the expression of TXS was mainly located in kytoplasm of cytotrophoblast,syncytiotrophoblast and few villus vascular endothelial cells in placenta. Preeclampsiagroup was stronger than control group and it has statistically significant differences(P<0.01).2.2the expression of TPr was mainly located in kytoplasm of cytotrophoblast,syncytiotrophoblast and villus vascular endothelial cells in placenta. It has nostatistically significant differences between preeclampsia group and control group(P>0.05).2.3the expression of NOX1was mainly located in kytoplasm of cytotrophoblast,syncytiotrophoblast, villus vascular endothelial cells and stroma cells in placenta.Preeclampsia group was stronger than control group and it has statistically significantdifferences (P<0.01).3. Real-Time PCR showed that3.1the expression of TXSmRNA in preeclampsia placenta was stronger than controlgroup and it has statistically significant differences (P<0.05).3.2the expression of TPrmRNA in preeclampsia placenta was tiny stronger thancontrol group, but it has no statistically significant differences between two groups(P>0.05).3.3the expression of NOX1mRNA in preeclampsia placenta was stronger than controlgroup and it has statistically significant differences (P<0.01).4. ELISA showed that4.1the expression of TXB2in preeclampsia placenta was stronger than control groupand it has statistically significant differences (P<0.05).4.2There were negative correlations between the expression of TXB2and neonatalbirth weight in preeclampsia (r=-0.446, P<0.01).4.3There were mild positive correlations between the expression of TXB2andNOX1mRNA in preeclampsia (r=0.367, P<0.05).Conclusion：TXA2which is the catalysate of TXS was improved by the increasedexpression of TXS in preeclampsia placenta. TXA2lead to placental ischemia andhypoxia by activate TPr. Then, the oxidative stress in placenta would followed. Simultaneity, TXA2may improve the expression of NOX1by activating TPr pathway.It lead a large amount of ROS was produced by placenta and released to maternalsystemic circulation. It participate in the progress of preeclampsia.