| Fetal growth restriction (FGR) is intituled intrauterine fetal growth retardation(IUGR),Which not only can influence on intrauterine growth of the fetus and also lead newborn to death.The fetus,matrix,environment,placenta and other danger factor all may lead to FGR,whereas the certain pathoqeny and pathoqenesis are still not fully understood. The supplies of the hematal circulation from placenta can influence on development of fetus in womb,and associate closely with vascular growth factor that express on placenta. In the pregnancy period,the the diversified factors from inner and outer entironment of matrix appear abnormal,which can reduce the blood stream and decline the prime may influence on development of fetus and cause FGR. This process may go with the change of the express of accelerate/contradict factor.Angiopoietin-2(Ang-2)is one of angiopoietins which has been newly found lately.It mainly expresses in womb、 placenta and other organs which can come into being blood vessels activityly. Ang-2is a differential stimulation factor which can creat blood vessels and has miqhtiness power that can promote creat blood vessels.Endoglin has anther name of CD105which is qlycoprotein that can stride cell membranet mainly express on cell membrane of human vascular endothelial and placenta cytotrophoblast. Endoglin is participate in producement and rebulitment blood vessel.Souble Endoglin is a factor which has strongly power of contradict producement blood vessel and rectify producement blood vessel.ObjectiveWe evaluate the function and clinic significance in pathogenesis of fetal growth restriction by observing the Ang-2, sEng levels of FGR in serm and in cord blood serum and the expression of Ang-2, Endoglin in placenta.Methods1Object:Choosing30full-term pregnant women being cesarean section in hospital with FGR as experiment group and30normal term pregnant women because of social factors terminating pregnancy as control group of Third Affiliated Hospital of Zhengzhou University from July2010to February2011.There is no other pregnancy complications and complications in all cases. All cases does not enter labor cesarean delivery before peration.2Methods:2.1Serum Specimen Collection:Blood serum samples came from sucking pregnant women vein blood5ml before caesarean operation and sucking umbilicus vein blood5ml after placenta being deliveried. Pregnant women vein blood and umbilicus vein blood samples were centrifugal by1000r/10min and remaining serum.2.2Placental Specimen Collection:Placenta form samples collected about1.0cm×1.0cm×1.0cm form from the center of the matrix side of placenta and avoiding bleeding and calcify and organization region. All the placenta form samples rainsed blood thoroughly by using physiological saline and fixed by10%formaldehyde solution, and then were embedded and sliced by pfraffin conventionally.2.3The enzyme-linked immunoadsordent assay (ELISA) was used to detect the levels of Ang-2, sEng in serum of pregnant women before cesarean section and the levels of Ang-2, sEng in umbilical cord serum after cesarean section. 2.4The immunohistochemistry staining and image analysis methods were used to detect the levels of Ang-2and Endoglin in placenta of pregnant women.3Statistics methodsSPSS13.0statistical analysis was employed to analyse all the data.All the data were showed by using mean±standard (x±s),using to test the comparison of the two enumerationdata groups,using Pearson linear correlation to analyze the two factors relativity analysis.Results1The comparison of the common data between the experimental group and the control group:The difference between the two groups of pregnant women in their ages,gestational weeks and pragnante degrees have no statistic meaning(P>0.05).2The expression of Ang-2,sEng in serm and Ang-2,Endoglin in the placenta of pregnant women of the experimental group and the control group:The levels of Ang-2in maternal serum (8.86±0.43) and The levels of Ang-2in umbilical cord serum(10.92±0.41)are lower in experimental group than that of control group (19.31±0.25,22.28±0.23), and the levels of sEng in maternal serum(4.63±0.09) and The levels of Ang-2in umbilical cord serum(5.06±0.10)are higher in experimental group than that of control group(2.77±0.09,2.97±0.09),and the expression of Ang-2(118.17±1.59)in placenta in experimental group is lower than that of Ang-2(151.64±1.64) in control group,and and the expression of Endoglin (106.04±1.12) in placenta in experimental group is higher than that of Endoglin (92.64±1.26) in control group,and all the differences were statistically significant (P <0.05).3The correlation between Ang-2, sEng and Endoglin in experimental group:The expression Ang-2in placenta were positively correlated to the levels in maternal serum in experimental group(r=0.930,P=0.000); The expression Ang-2in placenta were positively correlated to the levels in umbilical cord serum in experimental group(r=0.927,P=0.000); The levels of Ang-2maternal serum were positively correlated to the levels in umbilical cord serum(r=0.990,P=0.000); The expression level of Endoglin in placenta were positively correlated to the levels of sEng in maternal serum (r=0.880,P=0.000); The expression Endoglin in placenta were positively correlated to the levels of sEng in umbilical cord serum in experimental group(r=0.889,P=0.000); The levels of sEng in maternal serum were positively correlated to the levels in umbilical cord serum(r=0.961, P=0.000); There was no relationship between Ang-2and Endoglin in placenta(r=0.265, P=0.157).Conclusions1The level of Ang-2in maternal serum and umbilical cord serum and the expression level of Ang-2in placenta and are significant decrease may be related to the pathogenesis of FGR2The level of sEng in imaternal serum and the expression level of Endoglin in placenta and are significant heightening may participate in the development of FGR. |
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