摘要
目的:研究地塞米松对人类胎盘糖皮质激素受体前代谢酶11β-HSD2活性的调节作用,探讨产前应用地塞米松对妊娠和胎儿的影响,为临床防治早产和合理应用糖皮质激素提供理论依据。方法:利用改良的Kliman法分离提纯胎盘滋养细胞,原代培养3天后药物处理,用放射性酶活性结合薄层层析法(TLC)测定地塞米松对11β-HSD2氧化酶活性的调节作用。结果:体外实验条件下,培养的胎盘滋养层细胞具有11β-HSD2氧化酶活性,且与时间呈依赖关系。地塞米松作用于细胞4h、8h后,胎盘合体滋养细胞11β-HSD2的氧化酶活性明显降低,但孵育24h后,酶活性无明显变化。结论:地塞米松可显著降低胎盘合体滋养细胞11β-HSD2的氧化酶活性,可能是地塞米松、对胎儿有不良影响的重要机制之一,因此产前应用地塞米松必须慎重。
Objective： To study the effect of dexamethasone on glucocorticoids prereceptor metabolizing enzyme 11β-hydroxysteroid dehydrogenase type 2 （11β-HSD2） in human placental trophoblastic cells, aiming to theoretically elucidate relations between antenatal glucocorticoids and their side effects on pregnancy and fetuses. Methods： Human placentas were obtained from uncomplicated term pregnancy after elective caesarean section, placental trophoblastic cells were isolated using a modified method of Kliman. Trophoblastic cells were cultured in vitro for 3 days and treated with dexamethasone （DEX）. The activity of 11β-HSD2 was measured by radiometric conversion assay. Result： The activity of 11β-HSD2 of cultured trophoblastic cells was time-dependent. Treatment of trophoblasts with DEX significantly decreased 11β-HSD2 activity after 4 and 8 hours, but after 24 hours, 11β-HSD2 activity was not comparable between the two groups. Conclusions： In vitro, DEX can significantly suppress 11β-HSD2 oxidase activity, and the down-regulation of 11β-HSD2 oxidase induced by glucocorticoids would represent an important mechanism by which the fetuses might be suffered from exposure to elevated levels of maternal glucocorticoids.
出处
《现代妇产科进展》
CSCD
北大核心
2006年第12期921-923,共3页
Progress in Obstetrics and Gynecology
基金
国家自然科学基金资助课题(No:39970285)
上海市科技发展基金资助项目(No:99JC14036)
