Primer sequences of RT -qPCR.

BackgroundPolystyrene nanoparticles (PS-NPs) are recognized as environmental pollutants with potential reproductive toxicity. This study delves into the impacts of PS-NPs exposure on trophoblast cells, specifically examining mitochondrial dysfunction, cell invasion and migration.MethodsTrophoblast cells were exposed to PS-NPs to evaluate the effects on cell proliferation, apoptosis, mitochondrial function (including mitochondrial membrane potential, intracellular ROS levels, and gene expression), autophagy, inflammatory responses and cell motility. Co-immunoprecipitation and Western blotting analyses were employed to assess the expressions and interactions of MDM2 and ROCK1 under PS-NPs exposure conditions.ResultsWe observed that PS-NPs exposure impaired trophoblast cell proliferation, promoted apoptosis, and disrupted mitochondrial function, evident by ROS elevation, mitochondrial membrane potential reduction, and altered gene expression. Increased autophagy activity and inflammatory cytokine release indicated cellular stress. Moreover, PS-NPs impeded cell migration and invasion, with exacerbated effects upon MDM2 knockdown and ROCK1 inhibition.ConclusionThe study elucidates the intricate connections among mitochondrial dysfunction, autophagy, inflammation, and cell motility in response to PS-NPs, suggesting that targeting the MDM2-ROCK1 pathway could offer a promising approach to alleviate PS-NP-induced toxicity in trophoblast cells and support placental health.

背景：聚苯乙烯纳米颗粒（Polystyrene nanoparticles, PS-NPs）是一类被学界公认的具有潜在生殖毒性的环境污染物。本研究深入探讨了PS-NPs暴露对滋养层细胞的影响，重点考察线粒体功能障碍、细胞侵袭与迁移相关的细胞变化。
方法：研究人员将滋养层细胞暴露于PS-NPs环境中，以评估其对细胞增殖、凋亡、线粒体功能（涵盖线粒体膜电位、细胞内活性氧（ROS）水平及基因表达）、自噬、炎症反应与细胞运动能力的影响。同时采用免疫共沉淀（Co-immunoprecipitation）与蛋白质印迹（Western blotting）技术，分析PS-NPs暴露条件下MDM2与ROCK1的表达水平及其相互作用。
结果：研究结果显示，PS-NPs暴露会损伤滋养层细胞的增殖活性，促进细胞凋亡，并破坏线粒体功能，具体表现为ROS水平升高、线粒体膜电位降低以及基因表达出现异常改变。自噬活性增强与炎症细胞因子释放增加，提示细胞应激反应被激活。此外，PS-NPs会显著抑制细胞迁移与侵袭能力，且在MDM2敲低或ROCK1抑制的情况下，该抑制效应会进一步加重。
结论：本研究阐明了PS-NPs暴露下，线粒体功能障碍、自噬、炎症反应与细胞运动能力之间的复杂调控网络，提示靶向MDM2-ROCK1信号通路或可成为缓解PS-NPs诱导的滋养层细胞毒性、维护胎盘健康的潜在有效干预策略。