内毒素处理妊娠小鼠子宫组织一氧化氮与PGE2比值的变化。

Weiyue Zeng, Fang Yan, Yu Wang
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引用次数: 0

摘要

目的:探讨子宫组织一氧化氮与前列腺素E2比值与早产的关系。方法:孕鼠在妊娠第16天分别腹腔注射脂多糖(LPS)、脂多糖+ DETA/NO、脂多糖+ DETA或生理盐水。记录每只小鼠的给药时间。四组小鼠按照描述给予治疗。他们在12小时后被杀。测定血清黄体酮、子宫亚硝酸盐生成、PGE2。结果:lps处理小鼠子宫内亚硝酸盐和PGE2的生成明显高于对照组。相反,亚硝酸盐与PGE2的比值下降。DETA/NO可部分逆转血清孕酮水平的变化,而非DETA。结论:感染可通过改变一氧化氮与PGE2的比值诱发早产。一氧化氮可能通过减缓血清黄体酮的下降而阻止一氧化氮与PGE2比值的下降。并且可以预防脂多糖引起的早产。
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[The change of nitric oxide to PGE2 ratio in uterine tissues of endotoxin-treated pregnant mice].

Objective: To investigate the relationship between preterm labour 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, uterine production of nitrite and PGE2 were measured.

Results: Uterin production of nitrite and PGE2 in LPS-treated mice was significantly higher than that in control mice. In contrast the ratio of nitrite to PGE2 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 PGE2. Nitric oxide can prevent the decrease of nitric oxide to PGE2 ratio possibly by attenuating the fall of serum progesterone. And it can prevent LPS-induced preterm labor.

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