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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Cyclooxygenase inhibitors for treating preterm labour: What is the molecular evidence?
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Cyclooxygenase inhibitors for treating preterm labour: What is the molecular evidence?

机译：环加氧基酶抑制剂治疗早产劳动力：分子证据是什么？

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摘要

Preterm birth (<37 weeks of gestation) significantly increases the risk of neonatal mortality and morbidity. As many as half of all preterm births occur following spontaneous preterm labour. Since in such cases there are no known reasons for the initiation of labour, treatment of preterm labour (tocolysis) has sought to stop labour contractions and delay delivery. Despite some success, the use of cyclooxygenase (COX) inhibitors is associated with maternal/fetal side effects, and possibly increased risk of preterm birth. Clinical use of these drugs predates the collection of molecular and biochemical evidence in vitro, examining the expression and activity of COX enzymes in pregnant uterine tissues with and without labour. Such evidence is important to the rationale that COX enzymes are, or are not, appropriate targets for the tocolysis. The current study systematically searched existing scientific evidence to address the hypothesis that COX expression/activity is increased with the onset of human labour, in an effort to determine whether there is a rationale for the use of COX inhibitors as tocolytics. Our review identified 44 studies, but determined that there is insufficient evidence to support or refute a role of COX-1/-2 in the onset of preterm labour that supports COX-targeted tocolysis.
机译：早产（<37周的妊娠）显着提高新生儿死亡率和发病率的风险。在自发早产之后，所有早产的一半都发生了一半。由于在这种情况下，没有已知的劳动力发起的原因，因此需要停止劳动力劳动力的治疗（累累）阻止劳动收缩和延迟递送。尽管取得了一些成功，但使用环氧氧合酶（COX）抑制剂与母体/胎儿副作用有关，并且可能增加了早产的风险。这些药物的临床应用在体外预先收集分子和生化证据，检查孕妇子宫组织中Cox酶的表达和活性，无劳动。这些证据对核心酶是或不是适当靶向待溶解的适当靶标是重要的。目前的研究系统地搜查了现有的科学证据来解决核心人工劳动力发作增加Cox表达/活性的假设，以确定是否存在用于使用Cox抑制剂作为染色剂的理由。我们的审查确定了44项研究，但确定了不足以支持或反驳支持Cox靶向溶解的早产劳动力的Cox-1 / -2的作用。

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