Catechol estrogens stimulate synthesis of prostaglandins in the preimplantation rabbit blastocyst and endometrium.
Catechol estrogens stimulate synthesis of prostaglandins in the preimplantation rabbit blastocyst and endometrium.
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儿茶酚雌激素刺激植入前兔囊胚和子宫内膜中前列腺素的合成。
DOI：
10.1095/biolreprod29.2.347
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发表时间：
1983
影响因子：
3.6
通讯作者：
Dey,SK
中科院分区：
文献类型：
--
作者：
Pakrasi,PL;Dey,SK
本实验研究了雌二醇(E_2)或邻苯二酚雌二醇[4-羟基雌二醇-17-β(4-OH-E_2)或2-羟基雌二醇-17-β(2-OH-E_2)]对妊娠第6天(144h)兔胚泡和子宫内膜细胞前列腺素(PG)产生的影响。将囊胚(4~6枚)在1mlRPMI1640培养液中孵育8h，每隔2 h更换一次培养液，在−80℃下保存，第2、4期分别加入不同浓度的E2、4-OH-E2或2-OH-E2，第1、3期分别加入助剂。将子宫内膜组织单细胞悬液加入0.5mlRPMI-1640中，加入和不加入雌激素，孵育2 h。分离培养基及细胞，−80℃保存，放射免疫法测定PGs。囊胚的结果表现为在相同实验条件下两次孵育2小时内累积释放的PGs(PG/囊胚每4小时)。8.8M的4-OH-E_2对胚泡PGs的释放没有影响，而44µM的4-OH-E_2可使PGE-A的释放增加约25%，PGF的释放增加59%(P<；0.05)。在44µM的2-OH-E2存在下，PGE-A和PGF的释放分别被刺激约60%和37%。另一方面，任何浓度的E2对胚泡释放PGs均无影响或有抑制作用。与赋形剂对照组相比，4-OH-E2或2-OH-E2均可刺激子宫内膜细胞产生PGs(每2小时ng/mg蛋白)(P<；0.05)。与赋形剂对照组(PGF：18.90±0.82，PGE-A：2.18±0.22 ng)相比，17.6、44和88µM浓度的4-OH-E2分别使PGF和PGE-A的产量分别增加约111%、183%和221%和85%、144%和212%。17.6 mM和44 mM浓度的2-OH-E2对子宫内膜细胞产生PGF的刺激作用分别为67%和100%，而PGE-A的产生分别比对照组高126%和179%。另一方面，不同浓度的E2对子宫内膜细胞PGs的生成无影响或有抑制作用。结果表明，在所使用的剂量水平上，邻苯二酚雌二醇，而不是E2，在体外刺激着床前胚泡和子宫内膜细胞中PG的产生。
The influence of estradiol-17β(E2) or catechol estradiols [4-hydroxyestradiol-17β(4-OH-E2) or 2-hydroxyestradiol-17β(2-OH-E2)] on prostaglandin (PG) production in the rabbit blastocyst and endometrial cell in vitro on Day 6 of pregnancy (144 h postcoitum) was studied. Blastocysts (4–6) were incubated in 1 ml of RPMI-1640 medium for a total period of 8 h. Media were changed every 2 h and stored at −80°C. E2, 4-OH-E2or 2-OH-E2at various concentrations were added during the second and fourth periods, while the vehicle was added during the first and third periods. Single cell suspensions of endometrial tissues in 0.5 ml of RPMI-1640 were incubated for 2 h with and without estrogens. The media and cells were separated and stored at −80°C. PGs were determined by radioimmunoassay. The results for blastocyst were expressed as the cumulative release of PGs over a period of two 2-h incubations of the same experimental conditions (pg/blastocyst per 4 h). The release of PGs from the blastocyst was not influenced by 8.8µM of 4-OH-E2, whereas 44µM of this steroid stimulated the release of PGE-A by about 25% and PGF by 59% (P<0.05) over the vehicle-treated controls. The release of PGE-A and PGF in the presence of 44µM of 2-OH-E2was stimulated by about 60% and 37%. On the other hand, E2at any concentration, either showed none or inhibitory effects on the release of PGs from the blastocyst. The production of PGs in the endometrial cells (ng/mg protein per 2 h) was stimulated (P<0.05) in the presence of both 4-OH-E2or 2-OH-E2as compared to vehicle-treated controls. 4-OH-E2at a concentration of either 17.6µM, 44µM or 88µM increased the production of PGF by about 111%, 183% or 221% and PGE-A by 85%, 144% or 212%, respectively, as compared to vehicle-treated controls (PGF: 18.90 ± 0.82, and PGE-A: 2.18 ± 0.22 ng). The stimulation of PGF production in the endometrial cells by 2-OH-E2at 17.6 MM or 44 MM concentration was 67% or 100%, while the production of PGE-A was 126% or 179% more over the controls. On the other hand, E2at various concentrations either showed none or inhibitory effects on the production of PGs in the endometrial cells. The results demonstrate that catechol estradiols, but not E2, at the dose levels used, stimulate PG production in vitro both in the preimplantation rabbit blastocyst and endometrial cell.