EFFECTS OF THE ANTIPROGESTERONE RU-486 ON PRETERM BIRTH IN THE RAT
EFFECTS OF THE ANTIPROGESTERONE RU-486 ON PRETERM BIRTH IN THE RAT
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DOI：
10.1016/s0002-9378(87)80315-0
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发表时间：
1987-11-01
影响因子：
9.8
通讯作者：
BAULIEU, EE
中科院分区：
文献类型：
--
作者：
GARFIELD, RE;GASC, JM;BAULIEU, EE
在妊娠大鼠中研究了抗孕酮化合物RU 486对早产、子宫肌层缝隙连接和血浆类固醇激素水平的影响。在妊娠第16天注射RU 486导致24小时后开始延长分娩。RU 486引起的早产是伴随着子宫肌层细胞间缝隙连接的广泛发育而发生的。R5020，但无论是孕酮或地塞米松，防止早产和缝隙连接的发展。RU 486治疗后雌激素和孕酮水平下降，但仅在大部分胎儿分娩后。这项研究表明，孕酮可能通过抑制负责间隙连接表达的基因组来抑制子宫收缩。
The effects of the antiprogesterone compound RU 486 on preterm delivery, myometrial gap junctions, and plasma levels of steroid hormones were investigated in pregnant rats. Injection of RU 486 on day 16 of gestation resulted in prolonged delivery beginning after 24 hours. The preterm birth initiated by RU 486 was peceded and accompanied by the extensive development of gap junctions between myometrial cells. R 5020, but neither progesterone nor dexamethasone, prevented preterm birth and the development of gap junctions. Estrogen and progesterone levels declined after RU 486 treatment but only after a major proportion of the fetuses were delivered. This study indicates that progesterone may normally inhibit uterine contractility by suppressing the genome responsible for the expression of gap junctions.