米菲司酮对一氧化氮刺激小鼠子宫组织合成PGE_2的调节作用

RU486's Modulating Effect on the PGE_2 Generating Ability of Uterine Tissues of Mice in Response to Nitric Oxide

为探讨孕激素受体拮抗剂米菲司酮是否能调节子宫组织中一氧化氮 (nitric oxide,NO)和 PGE2 间的相互作用。给孕 16天的小鼠皮下注射米菲司酮或无水乙醇 ,12小时后处死小鼠 ,并将其子宫组织分别放入空白或含 IL- 1β、DETA/ NO或 DETA的 RPMI16 40培养液中培养。检测其子宫组织在培养液中产生的 PGE2 。结果 :与空白对照相比 ,两组小鼠的子宫组织在 DETA/ NO和 IL- 1β的刺激下 ,其 PGE2 生成量都增加。而在实验组 ,其增加幅度则更加显著 (2 8.5 1± 10 .6 7vs6 .85± 3.77,P<0 .0 1;5 3.38± 7.32 vs2 0 .6 1± 2 .93,P<0 .0 0 1)。这说明米菲司酮可以使 IL- 1β及 NO刺激子宫组织生成 PGE2 的作用加强。

This study was designed to investigate whether antiprogesterone RU486 could modulate the interactions between nitric oxide and prostaglandin E 2. The mice were injected subcutaneously with RU486 or vehicle on day 16 of gestation, and they were killed at 12 hours after the treatment. Their uterine tissues were incubated with or without IL 1β, DETA/NO, or DETA. The PGE 2 concentrations of the tissue culture medium were measured.The results showed whatever the mice were treated with before killed, their uterine tissues produced more PGE 2 when stimulated by IL 1β.The increment of PGE 2 in the uterine tissues of Ru486 treated mice was significantly higher than that of the mice treated with vehicle(28.51±10.67 vs. 6.85±3.77, P <0.01 ; 53.38±7.32 vs. 20.61±2.93, P <0.001). These findings indicate the increment of PGE2 production stimulated by IL 1β and nitric oxide in the uterine tissues can be expanded by Ru486.