| Pregnancy-induced Hypertension (PIH) as a pregnancy- dependant disease is a leading cause of fetal and maternal mortality and morbidity. Because its etiology and pathogenesis are undefined, there are no specific diagnostic test and efficient treatment. Untill now PIH is still one of the most important subject in perinatology. The placenta plays a central role in the pathogenesis of PIH, as removal of this organ at delivery normally results in prompt resolution of the disease. At present, researchers suggust that PIH be closely associated with abnormality of placenta function due to shallow invasion into the maternal uterine by trophoblast.It has been demonstrated that invasive function of placentae trophoblast is impared, leading to insufficient trophoblast invasion of maternal spiral arteries and uterine myometrial portions, which results in placenta shallow anchoring, it is the central pathophysiologic event in PIH, but the concrete cause remains poorly understood.In normal pregnancy, successful human placentation depends on adequate transformation of the uteroplacentas circulation by extravillous trophoblast(EVT) proliferation,migration,and invasion into the maternal deciduas. Previous studies showed that TGF- and TNF- a is a major regulator of human trophoblast differentiation and invasion. Abnormal expression of TGF- ?and TNF- a in placenta in trophoblast may contribute to the development of PIH. AT first this study by using immunohistochemical staining determines expression of TGF-p3 and TGF-P1 of the trophoblast and decidua of placenta obtained after delivery in the normal pregnancy and PIH pregnancy. At the same time, in vitro cultivating placenta villous of the normal pregnancy and the severe PIH obtained after delivery and respectively collecting supernatants in 1, 4, 12, 24 hours after cultivating, the concentration of TCP-P1 and TNF-a of placental trophoblast were measured by ELISA. The aim of the study is to demonstrate the role of TGF-pi , TGF-p3 and TNF-a in the pathogenesis of PIH , elucidate the etiology and pathogenesis of PIH, which provide the theoretic basis for working out treatment measures.Material and Method: Subjects in immunohistochemical stainingwere divided to two groups: 1. The PIH group(n=50,age of 24~35 years). According to the diagnostic standard ( OBSTETRICS AND GYNECOLOGY edited by lejie, the Fifth edition), it was further subdivided into mild(n=12), midden(n=18) and severe(n=20) group. All patients had no other complications of pregnancy, such as primary hypertension, renal disorders and infective diseases; 2. The normal group(n=30,age of 24-33 years). Women with normal pregnancy; Placental tissue of normal pregnancy and PIH were immediately obtained after delivery of placentas. The expression of TGF-P3 and TGF- 1 in placental tissue were determined by using immunohistochemical staining. Subjects in were divided to two groups: 1. The severe PIH group(n=6,age of 24-35 years). According to the diagnostic standard ( OBSTETRICS AND GYNECOLOGY edited by lejie, the Fifth edition). All patients had no other complications of pregnancy, such as primary hypertension, renal disorders and infective diseases; 2. The normal group(n=,age of 24-33 years), woman with normal pregnancy. In vitro cultivating placenta villous of the normal pregnancy and the severe PIH obtained after delivery and respectively collecting supernatants in 1, 4, 12, 24 hours after cultivating, the concentration of TCP-P1 and TNF-a of placental trophoblast were measured by ELISA. All experimental data were analysed with chi-square test, ANOVA or t test and processed by SPSS 10.0. There was a statistical significance when P<0.05.Results: 1. There was no significant difference between the PIHgroup and the normal group in maternal age, laboring gestational age,laboring mode and the use of pitocin during laboring. The weight of fetus in the PIH group was significnantly less than that of the normal group (P<0.05) . Systolic blood pressure(SBP) and diatolic blood pressure(DBP) in the PIH group were s...
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