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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。
To investigate whether the progestin receptor antagonist may affect the interaction between nitric oxide (NO) and PGE2 in uterine tissue. Mice of 16 days pregnant were subcutaneously injected with either Mifepristone or absolute ethanol. Mice were sacrificed after 12 hours and their uterus tissues were placed in blank or RPMI 1640 medium containing IL-1β, DETA / NO or DETA, respectively In training. Detect the uterine tissue produced in the culture medium PGE2. Results: Compared with the blank control, the uterine tissues of both groups increased their PGE2 production under the stimulation of DETA / NO and IL-1β. In the experimental group, the increase was more significant (2 8.51 ± 10.67 vs6.85 ± 3.77, P <0.01; 5 3.38 ± 7.32 vs 2.06 ± 2 .93, P <0. 0 0 1). This shows that the effect of nifedipine on IL-1β and NO stimulation of uterine tissue to produce PGE2 enhanced.