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甲状腺功能减退症中的胎儿生长受限与胎盘的增殖活性、细胞凋亡和血管生成变化有关。

Fetal growth restriction in hypothyroidism is associated with changes in proliferative activity, apoptosis and vascularisation of the placenta.

作者信息

Silva Juneo F, Vidigal Paula N, Galvão Daniele D, Boeloni Jankerle N, Nunes Philipe Pimenta, Ocarino Natália M, Nascimento Ernane F, Serakides Rogéria

机构信息

Departamento de Clínica e Cirurgia Veterinária, Escola de Veterinária, Universidade Federal de Minas Gerais. 31270-901 Belo Horizonte, MG, Brazil.

出版信息

Reprod Fertil Dev. 2012;24(7):923-31. doi: 10.1071/RD11219.

Abstract

The objective of this study was to evaluate fetal weight, histomorphometric changes and proliferative activity, apoptosis and angiogenesis of the placenta in rats with hypothyroidism. Thirty-six adult female rats were divided into two groups with 18 animals each: control and hypothyroidism. Hypothyroidism was induced by daily administration of propylthiouracil (1 mg/animal). The administration began five days before becoming pregnant and the animals were sacrificed at 14 or 19 days of gestation. The control group received a placebo. The number and weight of fetuses and the rate of fetal death was determined, as well as the morphometric characteristics, the immunohistochemical expression of cell division control protein 47 (CDC)-47 and vascular endothelial growth factor (VEGF) and the number of apoptotic cells in the placental disk. The data were analysed by Mann-Whitney U test. Hypothyroidism reduced the weight of fetuses and of the uterus and placenta (P<0.05), altered the thickness of the placental labyrinth and spongiotrophoblast (P<0.05), increased the population of glycogen cells in the spongiotrophoblast (P<0.05), interfered with the vascular development of the placental labyrinth and decreased VEGF expression (P<0.05), reduced the expression of CDC-47 and cellularity and increased the apoptotic rate in the placental disk (P<0.05). We conclude that hypothyroidism affects fetal weight by altering the proliferative activity, apoptosis and vascularisation of the placenta.

摘要

本研究的目的是评估甲状腺功能减退大鼠的胎儿体重、组织形态计量学变化以及胎盘的增殖活性、细胞凋亡和血管生成情况。36只成年雌性大鼠被分为两组,每组18只:对照组和甲状腺功能减退组。通过每日给予丙硫氧嘧啶(1毫克/只动物)诱导甲状腺功能减退。给药在怀孕前5天开始,动物在妊娠14天或19天时处死。对照组接受安慰剂。测定胎儿的数量和体重以及胎儿死亡率,以及胎盘盘的形态计量学特征、细胞分裂控制蛋白47(CDC)-47和血管内皮生长因子(VEGF)的免疫组化表达以及凋亡细胞数量。数据采用曼-惠特尼U检验进行分析。甲状腺功能减退降低了胎儿、子宫和胎盘的重量(P<0.05),改变了胎盘迷路和海绵滋养层的厚度(P<0.05),增加了海绵滋养层中糖原细胞的数量(P<0.05),干扰了胎盘迷路的血管发育并降低了VEGF表达(P<0.05),降低了CDC-47的表达和细胞密度,并增加了胎盘盘中的凋亡率(P<0.05)。我们得出结论,甲状腺功能减退通过改变胎盘的增殖活性、细胞凋亡和血管化来影响胎儿体重。

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