Prenatal depression is one of the most common psychological disorders during pregnancy, with an incidence of approximately 19.7% in China, and the incidence is showing a significant upward trend. Prenatal depression seriously endangers maternal and infant health, may lead to self-injury and suicide, and has lasting effects on the health of offspring. Studies have shown that gut microbiota imbalance and disruption of the gut-brain axis can affect brain function and behavior and play an important role in the occurrence and development of depression. Significant changes occur in the gut microbiota of pregnant women during pregnancy, which may influence inflammation and metabolism. Gut microbiota play a key role in tryptophan metabolism; however, the mechanisms by which maternal gut microbiota regulate tryptophan metabolism to affect brain function and mood remain unclear. This study aims to clarify the role of plasma tryptophan in the relationship between gut microbiota and prenatal depression in pregnant women based on the gut-brain axis mechanism. A total of 73 pregnant women were included in the study. The Edinburgh Postnatal Depression Scale (EPDS) was used for assessment. According to the cutoff score (10 points), participants were divided into a prenatal depression group (pregnant women with prenatal depression) and a control group (pregnant women without prenatal depression). Demographic information, fecal samples, and plasma samples were collected. Gut microbiota sequencing was performed using 16S ribosomal RNA (rRNA) sequencing. Amino acid detection in plasma and feces was conducted using ultrahigh performance liquid chromatography-electrospray ionization tandem mass spectrometry (UHPLC-ESI-MS/MS). Data were analyzed using SPSS 26.0 and R software, and mediation model analysis was performed using SPSS PROCESS. There were no statistically significant differences in α-diversity or β-diversity of gut microbiota between the 2 groups (all P>0.05). Compared with the control group, plasma tryptophan levels were significantly higher in the prenatal depression group (t=-2.964, P<0.05). The abundances of Candidatus_Soleaferrea (β=-19.945, OR<0.001, 95% CI <0.001 to 0.002, P=0.004) and Enterococcus (β=-9.074, OR<0.001, 95% CI <0.001 to 0.183, P=0.016) were negatively correlated with prenatal depression, whereas the abundance of Lachnospiraceae_NC2004_group was positively correlated with prenatal depression (β=5.870, OR=354.354, 95% CI 1.248 to 100 619.527, P=0.042). Plasma tryptophan levels played a mediating role between Enterococcus abundance and prenatal depression. Depressive symptoms during pregnancy are associated with the composition of gut microbiota during pregnancy. Tryptophan, as a precursor of serotonin, may play a mediating role in this process, providing new insights for improving prenatal depression through interventions targeting gut microbiota or tryptophan metabolism. 目的: 产前抑郁是孕妇在怀孕期间最常见的心理障碍之一，在中国发生率约为19.7%，且发生率呈显著上升趋势。产前抑郁严重危害母婴健康，可引起自伤、自杀，而且持续影响子代的健康。有研究表明肠道菌群失衡及肠-脑轴紊乱会影响大脑功能和行为，在抑郁的发生和发展中起重要作用。孕妇孕期的肠道菌群会发生显著变化，可能对炎症、代谢等方面产生影响。肠道菌群在色氨酸代谢中扮演关键角色，但孕妇肠道菌群调节色氨酸代谢影响大脑功能和情绪的机制尚未完全阐明。本研究旨在基于肠-脑轴机制阐明血浆色氨酸在孕妇肠道菌群与产前抑郁关联中的作用。方法: 共纳入73名孕妇进行研究，采用爱丁堡产后抑郁量表(Edinburgh Postpartum Depression Scale，EPDS)对孕妇进行评估，根据评分分界值(10分)将其分为产前抑郁组(产前抑郁的孕妇)及对照组(无产前抑郁的孕妇)。收集研究对象的相关人口统计信息、粪便和血浆样本。肠道菌群测序使用了16S核糖体RNA(ribosomal RNA，rRNA)测序，血浆和粪便的氨基酸检测使用了超高效液相色谱-电喷雾电离串联质谱分析(ultrahigh performance liquid chromatography-electrospray ionization tandem mass spectrometry，UHPLC-ESI-MS/MS)技术。采用SPSS 26.0和R软件进行数据分析，使用SPSS PROCESS进行中介模型分析。结果: 2组间肠道微生物群的α多样性和β多样性差异均无统计学意义(均P>0.05)。与对照组相比，产前抑郁组的血浆色氨酸含量显著升高(t=-2.964，P<0.05)。Candidatus_Soleaferrea (β=-19.945，OR<0.001，95% CI <0.001~0.002，P=0.004)和Enterococcus (β=-9.074，OR<0.001，95% CI <0.001~0.183，P=0.016)的丰度与产前抑郁均呈负相关，而Lachnospiraceae_NC2004_group的丰度与产前抑郁呈正相关(β=5.870，OR=354.354，95% CI 1.248~100 619.527，P=0.042)。血浆色氨酸水平在Enterococcus和产前抑郁之间起中介作用。结论: 孕期的抑郁症状与孕期肠道菌群的组成有关，而色氨酸作为5-羟色胺的前体物质，可能在这一过程中起中介作用，为今后通过肠道菌群或色氨酸代谢干预改善产前抑郁提供新思路。.
使用 AI 将内容摘要翻译为中文，便于快速阅读
使用 AI 分析这篇文章的核心发现、关键要点和深度见解
由 DeepSeek AI 提供分析 · 首次使用需配置 API Key
arXiv · 2025-06-06
arXiv · 2026-04-07