| Preeclampsia is a specific disease during pregnancy, characterized by maternal hypertension, proteinuria, and generalized edema, is a multicsystem disorder of human pregnancy that remains to this day the major cause of perinatal mortality and morbidity, There are 9.4 percents pregnancy women subject to the disease. Although the etiology of preeclampsia is poorly understood, there is accumulating evidence that a lack of trophoblast invasion of the placental bed spiral arteries leads to inadequate perfusion of the placenta and resultant hypoxia and pyslogical vessel rebuild barrier in preeclampsia.The latest rearch indicates that Insulin like growth factor- Ⅱ abbreviation IGF- Ⅱ is an important cytokine that can regulate various function of trophoblast abbreviation TB. IGF- Ⅱ is mainly producted by CTB and EVT. IGF- Ⅱ act an important role in trophoblast invasion. Classify and formation of placenta by auto crine and paracrine. The possible mechanism, which IGF-Ⅱ promote the trophoblast invasion is by promoting trophoblast crining matrix metalloproteinase(MMP), while MMP can promote the trophoblast invasion. The study on IGF- II expression in normal pregnancy and regulation to fetal growth very common, while the study on IGF-Ⅱ expression in preeclampsia serum and placenta is rarely. So the rearch for IGF-Ⅱ expression in preeclampsia is helpful to explore the reason for the abnormal function of trophoblast and further more to clarify the mechanism.This study analyze serum IGF- Ⅱ in maternal and unbilical cord between normal pregnancy and preeclampsia by ELISA. And at the same time the expression of IGF-Ⅱ in placenta was measured by immunohistochemistry. This rearch is to explore the relationship between IGF- Ⅱ and preeclampsia by observation the variety of IGF- Ⅱ in normal pregnancy and preeclampsia. There is no identical report in nation.Material and Methods: (1) All subject were devided into three groups: ①the normal third trimerter pregnant group (n=21); They are all healthy without other complications, ②mild preeclampsia (n=20): BP≥140/90mmHg, urinary protein≥ 300mg/24h or (+). ③severe preeclampsia (n=73): BP≥ 160/110mmHg, urinary protein ≥2.0g/24h. According to the diag nostic standard (OBSTETRICS AND GYNECOLOGY, the Sixth edit). All patients were of no other complications of pregnancy and primary hypertension, renal disorders. (2) Materal blood was obtained just before childbirth and umbilical cord blood was obtained a short after the placenta out of maternaity. The blood were all put in 37℃ for thirty minutes, then store the centrifugal serum in -20℃ until analysis. Immediately after the placental removal, the placental tissue was taken from the central and peripheral portion of the basal place as the size 1cm×1cm×1cm. These tissue samples was washed thoroughly in phosphate buffered saline, and immersed in 10% formaldehyde liquor until to analysis. The serum was measured by ELISA. And placental tissue was measured by immunohistochemisty SP.Results: (1) General clinic imformation. There is no significant difference in maternal ages gestational ages and foundational blood pressure between mild preeclampsia, severe preeclampsia and normal pregnancy (P<0.05); Mild and severe preeclampsia groups have significant higher blood pressure and urinary than the normal third trimester pregnancy group (p<0.05). (2) The dense of IGF-Ⅱ in maternal serum is significant higher in severe preeclampsia group than that of in mild preeclampsia and normal third trimester pregnancy groups (p<0.05), while there is no significant difference between mild preeclampsia and normal third trimester pregnancy groups (P>0.05). (3) The dense of IGF- Ⅱ in umbilical cord serum ismuch higher in severe preeclampsia group than that of in mild preeclampsia and both levels much higher than that of in normal third trimester pregnancy group (P<0.05). (4) The deuse of IGF- Ⅱ in maternal serum is much higher than that of umbilical cord.(5) Expression of IGF- Ⅱ in severe pregnancy placentas was obviously lower than that of mild preeclampsia placentas (P<0.05), with both levels being signicantly lower than that of uncomplicate hypertonsion placentas (P<0.05)oConclusion: (1) Maternal and umbilical serum level of IGF-Ⅱ in womenwith preeclampsia was significant higher than the normal third trimester pregnant women and the alternation is associated with the severity of preeclampsia. (2) The expression of IGF- Ⅱ in preeclampsia placenta was significant lower than that of in normal third trimester pregnant women and the alternation is associated with the severity of preeclampsia. Lacking of IGF- Ⅱ in placenta, which causes cytotrophblast inadequate invasion, pyslogical vessel vebuild barrier, narrow vessel and resultant hypoxia in preeclampsia. The possible reason is that relative regulation factors interaction and negative stimalation. (3) The role of IGF- Ⅱ in the mechanism of preeclampsia pathology is needed to further research, such as IGF- Ⅱ in matermal and umbilical serum. IGF-Ⅱ has a significant increase in maternal serum, while it can't get through matermal-fetal interface and act on its role. IGF-Ⅱ increases significantly in umbilical serum, but it doesn't cause correspondingly increase in placenta. The possible reason, that IGF-Ⅱ is mainly crined by fetal liver, and if there is different structure from the IGF- Ⅱ in placenta, is next research.
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