Zhang X, Croy B A
Department of Obstetrics and Gynaecology, University of Calgary, Alberta, Canada.
Biol Reprod. 1996 Sep;55(3):519-24. doi: 10.1095/biolreprod55.3.519.
In the mouse, estrogen and progesterone are required to prime the uterus for decidual cell reaction (DCR) in response to an intraluminal stimulus and, once DCR is induced, progesterone is required to maintain DCR. However, some evidence indicates that certain nonprogestational steroid hormones may also be involved in regulating DCR. The present study determined whether androgen plays any role in DCR. Adult CD1 mice were ovariectomized and treated with a regimen of estradiol and progesterone to prime the uterus for DCR and to maintain DCR. Sesame oil was injected into the uterine lumen to induce DCR on Day 5 of the treatment. DCR was determined by deciduomal weight-the difference between the wet weights of oil-injected and noninjected uterine horns. Testosterone, given at 1 mg/day during Days 3-5, could not replace progesterone in priming the uterus for DCR. However, the same dose of testosterone given during Days 6-8 maintained DCR. Alkaline phosphatase activity, a bio-marker for DCR, was present in the deciduoma maintained by either progesterone or testosterone, although the distribution of this enzyme activity was more intense in the antimesometrial pole in progesterone-maintained deciduoma. A nonaromatizable androgen, 5 alpha-dihydrotestosterone (DHT), was also effective in maintaining DCR, and this action of DHT was blocked by an androgen receptor antagonist, hydroxyflutamide. The relative potency of DHT in maintaining DCR was similar to that of progesterone. However, the regression of the deciduoma appeared to be advanced in DHT-treated mice. Ovariectomy on Day 6 of pregnancy resulted in resorption of the conceptus and regression of the decidua within 48 h. Treatment with DHT at the time of ovariectomy could not prevent fetal resorption, but it delayed the regression of decidua, as indicated, in part, by the presence of granulated metrial gland cells. In summary, androgen cannot prime the uterus for DCR, but it can maintain DCR once it is induced. The physiological significance of this finding remains to be determined.
在小鼠中，雌激素和孕酮是启动子宫对腔内刺激产生蜕膜细胞反应（DCR）所必需的，并且一旦诱导出DCR，就需要孕酮来维持DCR。然而，一些证据表明某些非孕甾体激素也可能参与调节DCR。本研究确定雄激素在DCR中是否发挥任何作用。将成年CD1小鼠去卵巢，并用雌二醇和孕酮方案进行处理，以使子宫对DCR启动并维持DCR。在处理的第5天，将芝麻油注入子宫腔以诱导DCR。通过蜕膜重量来确定DCR，即注射油的子宫角与未注射油的子宫角湿重之差。在第3 - 5天每天给予1mg睾酮，不能替代孕酮启动子宫对DCR的反应。然而，在第6 - 8天给予相同剂量的睾酮可维持DCR。碱性磷酸酶活性是DCR的一种生物标志物，在由孕酮或睾酮维持的蜕膜中均有存在，尽管这种酶活性的分布在孕酮维持的蜕膜中在反系膜极更为强烈。一种不可芳香化的雄激素，5α - 双氢睾酮（DHT），在维持DCR方面也有效，并且DHT的这种作用被雄激素受体拮抗剂氟他胺阻断。DHT在维持DCR方面的相对效力与孕酮相似。然而，在DHT处理的小鼠中，蜕膜的消退似乎提前了。在妊娠第6天进行去卵巢导致胚胎吸收，并且在48小时内蜕膜消退。在去卵巢时用DHT处理不能防止胎儿吸收，但它延迟了蜕膜的消退，部分表现为颗粒状子宫腺细胞的存在。总之，雄激素不能启动子宫对DCR的反应，但一旦诱导出DCR，它可以维持DCR。这一发现的生理意义仍有待确定。
