Objective: Hypertensive disorders in pregnancy is a specific diseasehappening in the late pregnancy.It is the main cause to increase the mortalityof pregnant women and neonates, a serious threat to the health of pregnanciesand neonates. But so far the pathogenesis of gestational hypertension diseaseclearly has not yet been elucidated, current research suggests reasonablereasons may be related to vascular endothelial cell injury and dysfunction,abnormal nourish cells into myometrium, the immune imbalance, nutritionaldeficiency, genetic factors and insulin resistance and other factors. Vascularendothelial cell injury and dysfunction is a central part of the pregnancy-induced hypertension disease pathological changes, more and more studies hasfound that endothelial cell damage may be related to the endothelial cells ofthe inflammatory reaction and the activity of vascular active factor and insulinresistance. Vascular endothelial growth factor is a specific vascular growthfactor, by means of promoting angiogenesis, regulating vascular activesubstances released, maintain the development of normal pregnancy placentatissue. Platelet derived growth factor-AA can shrink blood vessels andchemotactic activity such as a variety of biological functions,it is a variety ofcell mitosis agent in the body,in cell proliferation and migration of vascularand repair tissue injury plays an important role. Monocyte chemotacticprotein-1has the potential of leukocyte chemotaxis and activation, andvascular inflammatory disease and atherosclerosis are closely related. Thepurpose of this paper is to through the research of the expressions of VEGF,PDGF-AA and MCP-1in placenta of preeclampsia patiens, discussing therelationship with pregnancy hypertension disease, providing theoretical basisfor HDCP prevention and treatment. Methods:1we random select thirty cases of normal pregnancy as control group,which with light preeclampsia and with severe preeclampsia as study groupfrom obstetric patients at the fourth affiliated hospital of Hebei medicaluniversity from February2012to June2013(these cases withoutcomplications of internal medicine and other complications of pregnancy).2The specimen were collected from central placenta after the placentawas deliveried in30minutes from cesarean in pregnancy women about1cm×1cm×1cm(avoiding ischemia and calcification area), which was washedwith normal saline. Then they were fixed in10%formalin24h-48h.Conventional dehydration, paraffin, paraffin embedding, chiping themconsecutively in size4μm thick. Detect the expressions of VEGF, PDGF-AA, MCP-1in placenta by immunochemical SP method, according to thenumber of positive cells and intracellular staining intensity scale.3All the data was analyzed by SPSS13.0software wrap. measurementdata use single factor variance analysis, numeration data use χ2test, thecorrelation analysis between the two variables use Spearman grade relationanalysis. With P=0.05as significant standard.Results:1Clinical data contrast: There were no statistical difference betweencontrol and study group in age and gestational age (P>0.05).2The expression of VEGF2.1VEGF was mainly located in the membrane and cytoplasm ofplacental nourish cells and capillary vascular endothelial cells. Both incontrol group and study group, we can see tan particles. Positive expressionrate in control group in the placenta was86.67%,in study group was53.33%, there were significant statistical differences between them(P=0.002). The positive expression in light preeclampsia group was66.67%,in severe preeclampsia was40%, there were statistical differences(P=0.038). There were no statistical differences between control group andlight preeclampsia (P=0.067). There were statistical differences between control group and severe preeclampsia (P=0.000).2.2The expression of VEGF was decreased in study group contractingwith the control group, the expression was lower in severe preeclampsia thanin light preeclampsia.So thinking, the expression of VEGF had adecreasing tendency following up the development of the hypertensivedisorders in pregnancy.3The expression of PDGF-AA3.1PDGF-AA was mainly located in the membrane and cytoplasm ofplacental nourish cells and capillary vascular endothelial cells. There weretan particles in control group and study group. Positive expression rate incontrol group was63.33%, in study group was88.33%, there werestatistical differences between them (P=0.005). The positive expression inlight preeclampsia group was83.33%, in severe preeclampsia was93.33%,there were no statistical differences (P=0.228). There were no statisticaldifferences between control group and light preeclampsia (P=0.08). Therewere statistical differences between control group and severe preeclampsia(P=0.005).3.2The expression of PDFG-AA was ascended in study group, theexpression was higher in severe preeclampsia than in light preeclampsia.Sothinking,the expression of PDGF-AA had a increasing tendency followingup the development of the hypertensive disorders in pregnancy.4The expression of MCP-14.1MCP-1was expressed in the cytoplasm of the placenta trophocyte.There were tan particles in control group and study group in the cytoplasmof trophocyte in placenta. Positive expression rate in control groupwas36.67%,in study group was83.33%, there were statistical differencesbetween them (P=0.000). The positive expression in light preeclampsiagroup was76.67%, in severe preeclampsia was90.00%, there were nostatistical differences (P=0.166). There were statistical differences betweencontrol group and light preeclampsia (P<0.05). There were statisticaldifferences between control group and severe preeclampsia (P=0.006). 4.2The expression of MCP-1was ascended in study group, theexpression was higher in severe preeclampsia than in light preeclampsia.Sothinking,the expression of MCP-1had a increasing tendency following upthe development of the hypertensive disorders in pregnancy.5The expression of MCP-1in placenta was positive correlate to PDGF-AA, was negative correlate to VEGF.Conclusion:1The expression of VEGF had a decreasing tendency following up theseverity degree of hypertensive disorders in pregnancy, while the expressionof PDGF-AA and MCP-1had a increasing tendency following up thedevelopment of hypertensive disorders in pregnancy. It is proved thatVEGF, PDGF-AA, MCP-1play a role in the pathogenesis of hypertensivedisorders in pregnancy, and have relationship with the severity degree ofhypertensive disorders in pregnancy.2Patients with gestational hypertension disease due to placentaischemic anoxia, triggered a series of inflammatory reaction, the expressioninflammatory cytokines like PDGF-AA〠MCP-1increased,VEGFdecreased. Vascular endothelial cell damage,further aggravate gestationalhypertension disease progression.3The expression of MCP-1in placenta was positive correlated toPDGF-AA, was negative correlated to VEGF. They may correlate eachother, parting in the development of hypertensive disorders in pregnancy. |