| Objective: Hypertensive disorders in pregnancy is a specific disease inpregnancy, it is is the major cause resulting in morbidity and mortality inpregnant women and neonates. At present, there is no uniform measure for theetiology and pathological mechanism of hypertensive disorders in pregnancy.The causes be generally acknowledged, which influence each other,are activationand injury of vascular endothelium, immunity mechanism, the muscle of uteruswas invasived by abnormality trophoblast and heredity. In recent years,it isreported that activation and injury of vascular endothelium and immunitymechanism play an important role of the pathological change of the hypertensivedisorders in pregnancy. Interleukin-l (IL-1)is a inflammatory cytokine whichplays a vital role in regulating immunological reactions and mediatinginflammatory reactions. Vascular cell adhesion molecules-1(VCAM-1) mediatesthe adhesion and migration of T lymphocyte, monocyte,natural killer and soon, and play a role in inflammation regulation and immunologic process.VCAM-1is the marker of activation of vascular endothelium. Endoglin is one ofhomodimeric transmembrane glycoprotein. Through immunohistochemicalstaining SP to examine the relative expression of IL-1,VCAM-1and Endoglinin placenta, analyze the relationship with hypertensive disorders in pregnancy,and study the mechanism of IL-1,VCAM-1and Endoglin in hypertensivedisorders in pregnancy.Methods:1We selected a total of45cases of obstetric patients with hypertensivedisorders in pregnancy as study group at the fourth affiliated hospital of Hebeimedical university from September2010to September2011,of which thereare15cases with light preeclampsia,30cases with severe preeclampsia,andat the same period,we selected30cases with normal pregnancy as control group.(these pregnant woman without complications of internalmedicine andother complications of pregnancy)2About1cm×1cm×1cm specimen was collected from central placentaafter the placenta was deliveried in30minutes and was washed with normalsaline.Then they were fixed in10%formalin and24h later embedded inparaffin. Chip them consecutively in the size4μm thick. The expression ofIL-1β,VCAM-1and Endoglin in placenta was detected by immuno-histochemical SP method. Through immunohistochemical staining SP toexamine the expression of IL-1β,VCAM-1and Endoglin in placenta.3All the data was analyzed by SPSS13.0software wrap, measurementdata use single factor variance analysis,numeration data use χ~2test,ranked data use Wilcoxon signed-rank test,and Spearman grade relationanalysis, With a=0.05as significant standard.Results:1there were no statistical difference between control and study group inage and gestational age(p>0.05).2The expression of IL-1β2.1IL-1βwas expressed in the cytoplasm of syneytiotrophoblast inplacenta. Positive expression rates of IL-1β in control group and studygroup were73.33%and93.33%,there were no significant statisticaldifferences between them(Χ~2=6.923, p=0.009<0.05). The positiveexpression of IL-1βin light preeclampsia group was90.00%,it was nodifference significant than control group(Χ~2=2.783,p=0.095＞0.05). Thepositive expression of IL-1βin severe preeclampsia group was96.67%andit was no difference significant than light preeclampsia group (Χ~2=1.071,p=0.301＞0.05).2.2The expression of IL-1β in light preeclampsia group is higherthan that in control group(Z=-2.253,P=0.024<0.05). The expression in severepreeclampsia group is higher than that in control group (Z=-2.225,P=0.026<0.05).The expression of IL-1βhad increasing tendency follow upthe severity degree of patient's condition. 3The expression of VCAM-13.1VCAM-1was mainly located in the membrane and cytoplasm ofplacental villus syncytiotrophoblast and capillary vascular endothelial cells.Inthe control group VCAM-1was mainly located in syncytiotrophoblast and instudy group VCAM-1was mainly located in capillary vascular endothelialcells.Positive expression rates of VCAM-1located in placentalsyncytiotrophoblast in control group and study group were80.00%, and46.67%,there were significant statistical differences between them (Χ2=4.747,P=0.029<0.05). The positive expression in light preeclampsia groupwas56.67%,it was no difference significant than control group(Χ~2=3.774,P=0.052>0.05). The positive expression in severe preeclampsia group was36.67%and it was no difference significant than light preeclampsia group(Χ~2=2.411,P=0.121>0.05). Positive expression rates of VCAM-1located incapillary vascular endothelial cells in control group and study group were46.67%%, and76.67%,there were significant statistical differences betweenthem (Χ~2=8.110, P=0.004<0.05). The positive expression in lightpreeclampsia group was66.67%,it was no difference significant than controlgroup(Χ~2=1.684, P=0.194>0.05). The positive expression in severepreeclampsia group was86.67%and it was no difference significant thanlight preeclampsia group (Χ~2=3.354,P=0.067>0.05).3.2The expression of VCAM-1located in placental syncytiotrophoblastin light preeclampsia group is lower than that in control group(Z=-2.351,p=0.019<0.05). The expression in severe preeclampsia group is lower thanthat in control group(Z=-1.992,p=0.046<0.05).The expression of VCAM-1located in placental syncytiotrophoblast had decreasing tendency follow up theseverity degree of patient's condition.4The expression of Endoglin4.1Endoglin was mainly expressed in the membrane ofsyneytiotrophoblast in placenta. Positive expression rates of Endoglin in lightpreeclampsia group was73.33%,and in control group it was36.67%.The positive expression in light preeclampsia group was higher than that was incontrol group(Χ~2=8.148,p=0.004<0.05). The positive expression in severepreeclampsia group was86.67%and it was difference significant than lightpreeclampsia group (Χ~2=1.667,p=0.197＞0.05).4.2The expression of Endoglin in light preeclampsia group is higherthan that in control group(Z=-2.949,P=0.003<0.05). The expression in severepreeclampsia group is higher than that in control group (Z=-2.336,p=0.015<0.05).The expression of Endoglin had increasing tendencyfollow up the severity degree of patient's condition.5IL-1βand Endoglin were mainly expressed in syneytiotrophoblast ofplacenta.They compared with the expression of VCAM-1located insyncytiotrophoblast. IL-1βwas positive correlate to Endoglin, VCAM-1wasnegative correlate to IL-1βand Endoglin.Conclusion:1There are different expressions of IL-1β, VCAM-1and Endoglinprotein in control group,light preeclampsia group and severe preeclampsiagroup.2The expression of IL-1β and Endoglin in placenta hadincreasing tendency follow up the severity degree of hypertensive disorders inpregnancy,and the expression of VCAM-1located in placentalsyncytiotrophoblast had decreasing tendency follow up the severity degree ofcondition. Positive expression rates of VCAM-1located in capillary vascularendothelial cells in control group were higher than the study group. It isproved that IL-1β,VCAM-1and Endoglin play a role in the pothogenesy ofhypertensive disorders in pregnancy and have relatoinsip with the severitydegree of hypertensive disorders in pregnancy.3High expression of IL-1β in placenta of the patients withhypertensive disorders in pregnancy can promote the decidual cellsbiosynthesis prostaglandins, and activate the endothelial cells, inductionVCAM-1express high in endothelial cells, participate in the vascularendothelial cell injury. Although different mechanism, Endoglin also participate in endothelial cell injury; IL-1β and VCAM-1may affect theerosion of trophoblastic cells, participation in the pothogenesy ofhypertensive disorders in pregnancy.4IL-1βwas positive correlate to Endoglin in placenta and bothparticipate in the vascular endothelial cell injury,there may be synergisticrelation between them. IL-1βwas negative correlate to VCAM-1located insyncytiotrophoblast, both may influence each other, affect the erosion oftrophoblastic cells. IL-1β,VCAM-1and Endoglin effect each other and playa role in the pothogenesy of hypertensive disorders in pregnancy. |
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