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作 者:朱达琍[1] 田红[2] 胡艳群[2] 朱长虹[2]
机构地区:[1]江汉大学卫生技术学院,武汉430016 [2]华中科技大学同济医学院计划生育研究所
出 处:《中国计划生育学杂志》2007年第2期81-83,共3页Chinese Journal of Family Planning
基 金:国家高技术研究发展计划(863计划)课题(No.2002AA2Z3122)
摘 要:目的观察米非司酮对体外培养大鼠蜕膜组织的作用以及对蜕膜组织分泌纤溶酶原激活因子(PA)和血小板激活因子(PAF)的影响,探讨其抗早孕的作用机理。方法取妊娠大鼠蜕膜组织进行培养,设对照组、hCG组、受试药物组和hCG+受试药物组,观察米非司酮对早孕蜕膜组织分泌组织型纤溶酶原激活因子(tPA)及血小板激活因子-乙酰水解酶(PAF-AH)的影响。结果米非司酮能促进体外培养早孕蜕膜组织分泌tPA,同时使PAF-AH活性升高。结论提示米非司酮可能通过对PA、PAF的调节机制,抑制早孕的蜕膜反应,导致蜕膜发生不利于胚胎发育的组织变化达到抗早孕的药物作用。Objective : To observe the effect of mifepristone on the production of PA ( plasminogen activator) and PAF( platelet activating factor) in the rat's deciduas to probe into the antifertility mechanism. Methods: Three groups were observed which were control group, hCG( human chorionic gonadotropin) group and medication group with cultured decidua tissue. Results: Mifepristone could stimulate the production of tPA( tissue plasminogen activator) and PAF- AH( platelet activating factor acetylhydrolase) in cultured rat decidua tissue of early pregnancy as well as activate PAF - AH, and shorten the half - life of PAF. Conclusion: The antifertility effect of mifepristone might also be mediated by activating fibrinolysis of decidua, which leads to degeneration of decidua.
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