功能性孕激素撤退与分娩发动

Functional progesterone withdrawal and initiation of parturition

人类对分娩发动机制尚不清楚,因对分娩机制缺乏了解而无法主动选择合适时机计划分娩以降低母儿死亡率。目前,关于分娩发动机制有几种假说,其中功能性孕激素撤退学说因孕激素在妊娠中的重要作用而倍受关注,即人类分娩发动时局部组织孕激素的功能下调,而不是孕激素水平下降。孕激素受体-A/孕激素受体-B值升高是功能性孕激素撤退的基础,孕激素受体-B可上调孕激素激活基因的表达,而孕激素受体-A则下调孕激素的反应活性,即孕激素受体-A/孕激素受体-B值升高削弱孕激素对雌激素的调节性抑制作用,使得雌激素受体的表达增加,进而上调雌激素的功能及促收缩基因的表达,从而使子宫失去静止状态而诱发分娩。

The mechanisms of initiation of human parturition remain unknown.People can't choice reasonable opportunity to deliver to reduce maternal and neonatal mortalities because of our limited knowledge of the mechanisms involved.At present,there are several hypotheses,one of which,hypothesis of functional progesterone withdrawal is paid close attention because of importance of progesterone for pregnancy.The hypothesis is that when the human parturition is initiated,the function of progesterone is down-regulated rather than the level of progesterone is lowered.Increased ratio of progesterone receptor A (PR-A) to progesterone receptor B(PR-B) in the local tissues is basis of functional progesterone withdrawal.PR-B can up-regulate expression of progesterone receptor genes,while PR-A can down-regulate the activity of progesterone,that is to say,increased ratio of PR-A to PR-B weakens regulatory inhibition of progesterone on estrogen and increase expression of estrogen receptor α(ERα).The increased expression of ERα then up-regulates function of estrogen and expression of contraction associated genes,thus the uterus losses its static status and parturition is induced and initiated.