Endometrial prostaglandin E2 binding during the estrous cycle and its hormonal control in ovariectomized rats.
Endometrial prostaglandin E2 binding during the estrous cycle and its hormonal control in ovariectomized rats.
复制标题
子宫内膜前列腺素 E2 在动情周期中的结合及其对卵巢切除大鼠的激素控制。
DOI：
10.1095/biolreprod29.3.565
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发表时间：
1983
影响因子：
3.6
通讯作者：
A. Psychoyos
中科院分区：
文献类型：
--
作者：
T. Kennedy;D. Martel;A. Psychoyos
测定了[3H]前列腺素E2（[3H]PGE2）与子宫内膜制备物的结合，所述子宫内膜制备物是从处于发情周期的已知阶段的大鼠和用孕酮和雌二醇的各种组合治疗的卵巢切除大鼠获得的。没有具体的，高亲和力结合的[3H]PGE2可以检测到整个发情周期获得的子宫内膜制剂。在卵巢切除的大鼠用孕酮和雌二醇处理，以诱导中性，接受或postreceptive阶段的子宫内膜胚泡植入，最大浓度的子宫内膜PGE结合位点中发现的制剂从中性阶段。用雌二醇和黄体酮单独或联合治疗卵巢切除动物，发现子宫内膜PGE结合位点具有黄体酮依赖性，并且在开始黄体酮治疗后48小时首次可检测到。分离后的子宫内膜腔上皮细胞和基质在炔雌醇治疗的卵巢切除大鼠，PGE结合位点仅在基质膜制备。结果表明，大鼠子宫内膜PGE结合位点受激素控制，子宫内膜结合位点的浓度与子宫对蜕膜细胞反应的敏感性之间不存在简单的关系。
Binding of [3H] prostaglandin E2 ([3H]PGE2) to endometrial membrane preparations obtained from rats at known stages of the estrous cycle and from ovariectomized rats treated with various combinations of progesterone and estradiol was determined. No specific, high-affinity binding of [3H]PGE2 could be detected by endometrial membrane preparations obtained throughout the estrous cycle. In ovariectomized rats treated with progesterone and estradiol to induce either the neutral, receptive or postreceptive phase of the endometrium for blastocyst implantation, the greatest concentration of endometrial PGE binding sites was found in the preparations from the neutral phase. Treatment of ovariectomized animals with estradiol and progesterone, alone or combined, revealed that endometrial PGE binding sites were progesterone-dependent, and were first detectable 48 h after the initiation of progesterone treatment. Following separation of the endometrial luminal epithelium and stroma in progesterone-treated ovariectomized rats, PGE binding sites were detected only in the stromal membrane preparation. The results indicate the endometrial PGE binding sites in the rat are under hormonal control and that no simple relationship exists between the concentration of endometrial binding sites and uterine sensitization for the decidual cell reaction.