Effect of RU 486 on the endometrial response to deciduogenic stimulus in ovariectomized rhesus monkeys treated with oestrogen and progesterone.
Effect of RU 486 on the endometrial response to deciduogenic stimulus in ovariectomized rhesus monkeys treated with oestrogen and progesterone.
复制标题
RU 486 对接受雌激素和黄体酮治疗的去势恒河猴子宫内膜对蜕膜刺激的反应的影响。
DOI：
10.1093/oxfordjournals.humrep.a137792
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发表时间：
1992
影响因子：
6.1
通讯作者：
J. Sengupta
中科院分区：
文献类型：
--
作者：
D. Ghosh;P. De;J. Sengupta
采用恒河猴人工斑块-蜕膜细胞模型，通过时间调整应用抗孕激素RU 486，研究了孕酮在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袭滋养层细胞的直接反应。为了研究这一过程，RU 486(2.5 mg/kg体重)或赋形剂(乙醇/生理盐水，7：3，v/v，肌肉注射)在创伤后立即给第一组猴子(治疗周期的第16天和第17天)。组织计量学分析显示，与对照猴相比，RU486处理可显著抑制(P<0.001)上皮细胞向斑块腺泡内的聚集，从而减少斑块反应的扩散(P<0.001)。在第二组猴子中，实验治疗被推迟到斑块形成(周期的第21天和第22天)。RU-486诱导斑块细胞变性增加(P<0.01)。因此，上皮斑块反应的转化和维持似乎是孕激素依赖性的。RU-486处理后，腺上皮细胞的最大细胞高度、假复层数量和分泌活性仅有轻微变化(P<0.05)，但抗孕激素诱导的腺细胞凋亡率较高(两组均P<0.01)。RU-486的孕激素受体阻断作用可能导致腺上皮细胞出现较高程度的细胞凋亡。RU 486治疗后内皮细胞超微结构无明显变化，但静脉直径明显增大(P<0.001，I组；P<0.001，II组)，水肿程度明显减轻。经RU486治疗后，白细胞渗出增加(P<0.001.0 1)，白细胞渗出增加(P<0.0 5，P<0.0 5)。RU 486引起的血管反应和排尿增加可能是由于其对血管细胞的孕酮阻断作用所致。RU486可加速(P<0.001.0 1)间质蜕膜化的发生(P<0.0 1)，并定量增加(P<0.0 1)蜕膜细胞反应(P<0.0 1)。RU 486可能抑制蜕膜细胞的特定功能，尽管蜕膜转化形态一致。
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.