脂多糖诱发的早产小鼠子宫组织NO、PGE_2的变化

The Change of Nitric Oxide to PGE_2 Ratio in Uterine Tissues of Endotoxin-treated Pregnant Mice

目的 探讨感染性早产的发生与子宫局部组织一氧化氮 (NO)和前列腺素 (PGs)比值变化的关系。方法 将 2 0只孕 16天的小鼠分为脂多糖、脂多糖乙二胺四乙酸二钠 /一氧化氮 (DETA/ NO)、脂多糖 +DETA以及生理盐水组 4组 ,每组 5只 ,分别注药后观察它们的分娩时间 ,另外 4组孕鼠共 2 0只 ,在给予上述药物后 12小时处死 ,检测其血清孕酮水平及子宫组织产生的亚硝酸盐和 PGE2 。结果 给予脂多糖注射的孕鼠子宫组织产生亚硝酸盐及 PGE2 增加 ,而亚硝酸盐与 PGE2 的比值及其血清孕酮水平则明显下降。DETA/ NO可以部份逆转。结论 脂多糖可以通过使小鼠血清孕酮水平下降并使其子宫局部组织的 NO/ PGE2 值降低而诱发早产 ,DETA/ NO则可能通过阻止血清孕酮水平的下降以恢复局部组织的 NO/ PGE2 值 。

Objective To investigate the relationship between preterm labor and the ratio of nitric oxide to prostaglandin E2 in uterine tissues. Methods Pregnant mice were given lipopolysaccharide(LPS), LPS+DETA/NO, LPS+DETA or saline solution respectively by intraperitoneal injection on day 16 of gestation. The delivery time of each mouse was recorded. Four separate groups of mice were given treatment as described. And they were killed at 12 hours after that. Serum progesterone, uterin production of nitrite and PGE 2 were measured. Results Uterin production of nitrite and PGE 2 in LPS treated mice was significantly higher than that in control mice. In contrast the ratio of nitrite to PGE 2 decreased. Accompanied by the fall of serum progesterone level DETA/NO rather than DETA could partially reversed the changes. Conclusion Infection can induce preterm labor by altering the ratio of nitric oxide to PGE 2. Nitric oxide can prevent the decrease of nitric oxide to PGE 2 ratio possibly by attenuating the fall of serum progesterone. And it can prevent LPS induced preterm labor.