Ghosh D, De P, Sengupta J
Department of Physiology, All India Institute of Medical Sciences, New Delhi.
Hum Reprod. 1992 Sep;7(8):1048-60. doi: 10.1093/oxfordjournals.humrep.a137792.
Using the artificial plaque--decidual cell model in rhesus monkeys, the potential role of progesterone in the process of of epithelial and stromal cell responses was investigated by time-adjusted application of an antiprogestin, RU 486. Epithelial plaque formation is an immediate response of the endometrium to either trauma or invading trophoblast cells. To study this process, RU 486 (2.5 mg/kg body weight) or vehicle (ethanol/saline, 7:3, v/v, i.m.) was administered to the first group of monkeys immediately following traumatization (days 16 and 17 of treatment cycle). Histometric analysis revealed that treatment with RU 486 led to significant inhibition (P less than 0.001) in the recruitment of epithelial cells into plaque acini and consequent reduction (P less than 0.001) in the spread of the plaque reaction compared with control monkeys. In the second group of monkeys, experimental treatment was delayed until plaque formation had occurred (days 21 and 22 of cycle). RU 486 induced increased degeneration (P less than 0.01) in plaque cells. Thus the transformation and the maintenance of the epithelial plaque response appears to be progesterone-dependent. Glandular epithelium showed only marginal changes (P less than 0.05) in maximum cell height, amount of pseudostratification and secretory activity of glands as a consequence of RU 486 treatment; however, the antiprogestin induced a higher incidence of glandular apoptosis (P less than 0.01 for both groups). It has been suggested that the higher degree of apoptosis in the glandular epithelium could be a consequence of the progesterone receptor blocking action of RU 486. No distinctive change in endothelial cell ultrastructure was evident following RU 486 treatment; however, venular diameter was significantly increased (P less than 0.01, group I; P less than 0.001, group II) along with an apparent reduction in the extent of oedema. There was increased extravasation (P less than 0.01) and leukocytic infiltration (P less than 0.001, group I; P less than 0.05, group II) following RU 486 treatment. RU 486 induced vascular responses and increased diapedesis could presumably have resulted from its progesterone blocking action in vascular cells. RU 486 accelerated the incidence (P less than 0.01) of stromal decidualization (group I), as well as quantitatively accentuating (P less than 0.001) the decidual cell reaction (group II). It is possible that RU 486 may inhibit specific functions of decidual cells, despite morphologically consistent decidual transformation.
利用恒河猴的人工斑块 - 蜕膜细胞模型，通过适时应用抗孕激素RU 486，研究了孕酮在子宫内膜上皮细胞和基质细胞反应过程中的潜在作用。上皮斑块形成是子宫内膜对创伤或侵入的滋养层细胞的即时反应。为研究此过程，在创伤后（治疗周期的第16和17天）立即给第一组猴子注射RU 486（2.5mg/kg体重）或赋形剂（乙醇/盐水，7:3，v/v，肌肉注射）。组织计量学分析显示，与对照猴子相比，用RU 486治疗导致上皮细胞向斑块腺泡募集的显著抑制（P<0.001），并导致斑块反应扩散的相应减少（P<0.001）。在第二组猴子中，实验治疗延迟至斑块形成后（周期的第21和22天）进行。RU 486诱导斑块细胞变性增加（P<0.01）。因此，上皮斑块反应的转变和维持似乎依赖于孕酮。由于RU 486治疗，腺上皮在最大细胞高度、假复层程度和腺体分泌活性方面仅表现出轻微变化（P<0.05）；然而，抗孕激素诱导腺体凋亡的发生率更高（两组均为P<0.01）。有人认为，腺上皮中较高程度的凋亡可能是RU 486的孕酮受体阻断作用的结果。RU 486治疗后内皮细胞超微结构未见明显变化；然而，小静脉直径显著增加（第一组P<0.01；第二组P<0.001），同时水肿程度明显减轻。RU 486治疗后血管外渗增加（P<0.01）和白细胞浸润增加（第一组P<0.001；第二组P<0.05）。RU 486诱导的血管反应和增加的血细胞渗出可能是由于其在血管细胞中的孕酮阻断作用。RU 486加速了基质蜕膜化的发生率（第一组，P<0.01），并在数量上增强了蜕膜细胞反应（第二组，P<0.001）。尽管蜕膜细胞形态学上发生了一致的转变，但RU 486仍有可能抑制蜕膜细胞的特定功能。
