Jonsson H T, Rankin J C, Ledford B E, Baggett B
Prostaglandins. 1979 Dec;18(6):847-57. doi: 10.1016/0090-6980(79)90122-9.
Prostaglandin E (PGE) and F (PGF) levels were measured in mouse uteri at various times after either trauma (hemostat crusing) or oil stimulation of the decidual cell reaction (DCR). The oil induced DCR led to an early increase (within 5 min) in both PGE and PGF levels. Both returned to baseline by 1 h after stimulation. A second peak in PGF levels was observed at 120 min after oil stimulation. This study demonstrates a distinct difference between the pattern of PGE and PGF changes in the uterus following oil stimulation of the DCR. Indomethacin pretreatment completely blocked the oil stimulated DCR as well as all prostaglandin increases following either stimulus. The trauma stimulated DCR was not completely blocked by indomethacin pretreatment. Pretreatment with tranylcypromine, an inhibitor of prostacyclin biosynthesis, did not block the prostaglandin E and F increases, but did block the oil stimulated DCR. These findings suggest that prostacyclin may be an early mediator of the DCR.
在对蜕膜细胞反应(DCR)进行创伤(止血钳挤压)或油刺激后的不同时间,测量小鼠子宫中的前列腺素E(PGE)和F(PGF)水平。油诱导的DCR导致PGE和PGF水平在早期(5分钟内)升高。刺激后1小时两者均恢复至基线水平。油刺激后120分钟观察到PGF水平出现第二个峰值。本研究表明,油刺激DCR后子宫中PGE和PGF变化模式存在明显差异。吲哚美辛预处理完全阻断了油刺激的DCR以及两种刺激后所有前列腺素的升高。创伤刺激的DCR未被吲哚美辛预处理完全阻断。用前列环素生物合成抑制剂反苯环丙胺预处理并未阻断前列腺素E和F的升高,但确实阻断了油刺激的DCR。这些发现表明,前列环素可能是DCR的早期介质。