源自人脐带间充质干细胞（hucMSC-exos）的外泌体由于其调节细胞间信号通讯的能力而成为治疗各种疾病的新策略。然而，hucMSC-exos 改善产科抗磷脂综合征胎盘损伤的潜力及其潜在机制仍不清楚。我们的目的是探索 hucMSC-exos 在治疗产科抗磷脂综合征中的潜在应用并阐明其潜在机制。在我们的研究中，hucMSC-exos 通过传递 miR-146a-5p 改善了体外抗磷脂抗体引起的滋养细胞功能损伤，并减轻了产科抗磷脂综合征小鼠的胎盘功能障碍。外泌体miR-146a-5p抑制肿瘤坏死因子受体相关因子6（TRAF6）的表达并抑制NF-κB信号传导的激活，导致IL-1β和IL-18下调以拯救炎症和调节Cleaved-CASP3、BAX 和 BCL2 抑制 HTR8/SVneo 细胞和小鼠胎盘细胞凋亡。这项研究确定了 hucMSC-exos 如何改善抗磷脂抗体诱导的胎盘损伤的潜在分子基础，并强调了 miR-146a-5p/TRAF6 轴在产科抗磷脂综合征进展中的功能重要性。更重要的是，这项研究为 hucMSC-exos 作为产科抗磷脂综合征的一种新颖有效的治疗方法的前景提供了新的前景。© 2023。作者。

Exosomes originating from human umbilical cord mesenchymal stem cells (hucMSC-exos) have become a novel strategy for treating various diseases owing to their ability to regulate intercellular signal communication. However, the potential of hucMSC-exos to improve placental injury in obstetric antiphospholipid syndrome and its underlying mechanism remain unclear. Our objective was to explore the potential application of hucMSC-exos in the treatment of obstetric antiphospholipid syndrome and elucidate its underlying mechanism. In our study, hucMSC-exos ameliorated the functional impairment of trophoblasts caused by antiphospholipid antibodies in vitro and attenuated placental dysfunction in mice with obstetric antiphospholipid syndrome by delivering miR-146a-5p. Exosomal miR-146a-5p suppressed the expression of tumor necrosis factor receptor-associated factor 6 (TRAF6) and inhibited the activation of NF-κB signaling, leading to the down-regulation of IL-1β and IL-18 to rescue inflammation and modulation of Cleaved-CASP3, BAX, and BCL2 to inhibit apoptosis in HTR8/SVneo cells and mice placenta. This study identified the potential molecular basis of how hucMSC-exos improved antiphospholipid antibody-induced placental injury and highlighted the functional importance of the miR-146a-5p/TRAF6 axis in the progression of obstetric antiphospholipid syndrome. More importantly, this study provided a fresh outlook on the promising use of hucMSC-exos as a novel and effective treatment approach in obstetric antiphospholipid syndrome.© 2023. The Author(s).