Bosco C, Buffet C, Díaz E, Rodrigo R, Morales P, Barja P, Terra R, Parra-Cordero M
Anatomy and Developmental Biology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Chile.
Cardiovasc Hematol Agents Med Chem. 2010 Apr;8(2):87-95. doi: 10.2174/187152510791170951.
The pathophysiology of preeclampsia (PE), a disorder occurring in 5% of all pregnancies, remains largely unknown, but early placental hypoxia and oxidative stress are known to be involved in the mechanism of the syndrome. Maternal plasma and placental tissue samples were collected from PE, intrauterine growth restriction (IUGR), and normotensive pregnant patients. The immunohistochemical expression of vascular endothelial growth factor (VEGF), malondialdehyde (MDA) production and the activity of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase GSH-Px) were determined in the placental tissue. F2-isoprostane concentration and the ferric reducing ability of plasma (FRAP) were determined in maternal plasma. We found that the PE and IUGR groups showed a higher expression of VEGF in the muscular layer of fetal chorionic vessels. In addition, increased plasma F2 isoprostane levels and a significant reduction of FRAP in the plasma of PE women, as well as a lower activity of SOD in PE placentas and a higher activity of GSH-Px in IUGR placentas were found. Additionally, lower PlGF and higher sFlt1 levels were observed in the maternal plasma of PE and IUGR than control. We concluded that in a hypoxic environment, the placenta expresses VEGF in the muscular layer of fetal vessels. The development of PE could be related to the increased expression of VEGF, with decreased placental SOD activity and a decrease of both plasma F2-isoprostane and FRAP levels. In turn, the development of IUGR could be related to the association of decreased plasma FRAP levels and increased placental GSH-Px activity.
先兆子痫（PE）是一种在所有妊娠中发生率为5%的疾病，其病理生理学在很大程度上仍不清楚，但已知早期胎盘缺氧和氧化应激参与了该综合征的发病机制。从患有PE、胎儿宫内生长受限（IUGR）的孕妇以及血压正常的孕妇中采集母体血浆和胎盘组织样本。测定胎盘组织中血管内皮生长因子（VEGF）的免疫组化表达、丙二醛（MDA）的产生以及抗氧化酶（超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶GSH-Px）的活性。测定母体血浆中F2-异前列腺素浓度和血浆铁还原能力（FRAP）。我们发现，PE组和IUGR组在胎儿绒毛血管肌层中VEGF表达较高。此外还发现，PE孕妇血浆中F2-异前列腺素水平升高且FRAP显著降低，PE胎盘组织中SOD活性较低，而IUGR胎盘组织中GSH-Px活性较高。此外PE组和IUGR组孕妇母体血浆中胎盘生长因子（PlGF）水平较低而可溶性血管内皮生长因子受体1（sFlt1）水平较高。我们得出结论，在缺氧环境下，胎盘在胎儿血管肌层中表达VEGF。PE的发生可能与VEGF表达增加、胎盘SOD活性降低以及血浆F2-异前列腺素和FRAP水平降低有关。反过来，IUGR的发生可能与血浆FRAP水平降低和胎盘GSH-Px活性增加有关。
