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首页> 外文期刊>Cardiovascular & hematological agents in medicinal chemistry >VEGF in the muscular layer of placental blood vessels: immuno-expression in preeclampsia and intrauterine growth restriction and its association with the antioxidant status.
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VEGF in the muscular layer of placental blood vessels: immuno-expression in preeclampsia and intrauterine growth restriction and its association with the antioxidant status.

机译:胎盘血管肌肉层中的VEGF:子痫前期和子宫内生长受限的免疫表达及其与抗氧化剂状态的关系。

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摘要

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.
机译:子痫前期(PE)的病理生理学(在所有妊娠中占5%的疾病)仍然未知,但已知早期胎盘缺氧和氧化应激与该综合征的发病机制有关。从PE,宫内生长受限(IUGR)和血压正常的孕妇中收集孕妇血浆和胎盘组织样品。确定胎盘组织中血管内皮生长因子(VEGF)的免疫组织化学表达,丙二醛(MDA)的产生以及抗氧化酶的活性(超氧化物歧化酶,过氧化氢酶和谷胱甘肽过氧化物酶GSH-Px)。测定母体血浆中的F2-异前列腺素浓度和血浆铁还原能力(FRAP)。我们发现,PE和IUGR组在胎儿绒毛膜血管的肌肉层中显示出更高的VEGF表达。此外,发现PE妇女血浆中F2异前列腺素水平升高,FRAP显着降低,PE胎盘中SOD活性降低,IUGR胎盘中GSH-Px活性升高。另外,在PE和IUGR的母体血浆中观察到比对照更低的PlGF和更高的sFlt1水平。我们得出的结论是,在缺氧的环境中,胎盘在胎儿血管的肌肉层表达VEGF。 PE的发展可能与VEGF的表达增加,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的发展可能与血浆FRAP水平降低和胎盘GSH-Px活性升高有关。

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