背景:胎盘充当缓冲液,通过11-β羟基类固醇脱氢酶同工酶2型(11-βHSD2)酶调节胎儿暴露于母体皮质醇的程度。我们进行了系统评价和荟萃分析,以评估产前心理困扰(PPD)对胎盘11-βHSD2基因表达的影响,并探讨参与胎儿神经发育的相关机制途径。
方法:我们搜索了PubMed,Embase,Scopus,APAPsycInfo®,和ProQuest论文,用于评估人胎盘中PPD和11-βHSD2表达之间的相关性的观察性研究。调整后的回归系数(β)和相应的95%置信区间(CIs)基于三个上下文PPD暴露组进行汇总:产前抑郁,焦虑症状,和感知的压力。
结果:在检索到的3159条记录中,纳入了16项纵向研究,涉及7个国家的1869名参与者.总的来说,暴露于PPD疾病显示与胎盘11-βHSD2基因表达的弱负相关性如下:产前抑郁(β-0.01,95%CI0.05-0.02,I2=0%),焦虑症状(β-0.02,95%CI0.06-0.01,I2=0%),和感知压力(β-0.0195%CI0.06-0.04,I2=62.8%)。妊娠晚期PPD暴露更频繁地与胎盘11-βHSD2水平降低相关。PPD和胎盘11-βHSD2与皮质醇反应性的变化以及母亲和儿童不良健康结局的发展有关。雌性后代更容易受到PPD暴露。
结论:该研究表明,产前心理困扰在调节胎盘11-βHSD2基因表达中具有适度的作用。应计划使用更大的样本量或先进的统计方法来增强对小效应大小的检测的未来前瞻性队列。此外,控制关键预测因素,如母亲的种族,PPD暴露的三个月,交货方式,婴儿性别对于有效探索PPD对胎儿程序的影响至关重要。
BACKGROUND: The placenta acts as a buffer to regulate the degree of fetal exposure to maternal cortisol through the 11-Beta Hydroxysteroid Dehydrogenase isoenzyme type 2 (11-β HSD2) enzyme. We conducted a systematic
review and meta-analysis to assess the effect of prenatal psychological distress (PPD) on placental 11-β HSD2 gene expression and explore the related mechanistic pathways involved in fetal neurodevelopment.
METHODS: We searched PubMed, Embase, Scopus, APA PsycInfo®, and ProQuest Dissertations for observational studies assessing the association between PPD and 11-β HSD2 expression in human placentas. Adjusted regression coefficients (β) and corresponding 95% confidence intervals (CIs) were pooled based on three contextual PPD exposure groups: prenatal depression, anxiety symptoms, and perceived stress.
RESULTS: Of 3159 retrieved records, sixteen longitudinal studies involving 1869 participants across seven countries were included. Overall, exposure to PPD disorders showed weak negative associations with the placental 11-β HSD2 gene expression as follows: prenatal depression (β -0.01, 95% CI 0.05-0.02, I2=0%), anxiety symptoms (β -0.02, 95% CI 0.06-0.01, I2=0%), and perceived stress (β -0.01 95% CI 0.06-0.04, I2=62.8%). Third-trimester PPD exposure was more frequently associated with lower placental 11-β HSD2 levels. PPD and placental 11-β HSD2 were associated with changes in cortisol reactivity and the development of adverse health outcomes in mothers and children. Female-offspring were more vulnerable to PPD exposures.
CONCLUSIONS: The study presents evidence of a modest role of prenatal psychological distress in regulating placental 11-β HSD2 gene expression. Future prospective cohorts utilizing larger sample sizes or advanced statistical methods to enhance the detection of small effect sizes should be planned. Additionally, controlling for key predictors such as the mother\'s ethnicity, trimester of PPD exposure, mode of delivery, and infant sex is crucial for valid exploration of PPD effects on fetal programming.