School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan, 316022, China.
Zhoushan Institute for Food and Drug Control, Zhoushan, 316000, China.
Int Immunopharmacol. 2024 Dec 5;142(Pt A):113154. doi: 10.1016/j.intimp.2024.113154. Epub 2024 Sep 14.
Plastic pollution has become a global pollution problem that cannot be ignored. As the main destination of human oral intake, the toxic effects of plastic on the digestive system represented by the intestine and liver are the focus of current research. Marine-derived DHA-PS has a variety of biological activities, mainly focusing on improving brain function and regulating lipid metabolism. However, whether it has an improvement effect on PS-NPs-induced hepato-intestinal injury and the underlying mechanism remain unclear.
A murine liver injury model was established by gavage of PS-NPs for six weeks. By integrating approaches from lipidomics, transcriptomics, and gut microbiota analysis, the molecular mechanism by which DHA-PS alleviates PS-NPs-induced murine hepatotoxicity was explored through the "gut-liver axis".
Our findings reveal that prolonged exposure to PS-NPs results in significant murine liver damage and dysfunction, characterized by increased oxidative stress and inflammation, along with exacerbated hepatic lipid accumulation. Mechanistically, PS-NPs disrupt the hepatic SIRT1-AMPK pathway by suppressing the expression of SIRT1, AMPKα, and PPARα, while enhancing the expression of SREBP-1c, ultimately leading to disordered hepatic lipid metabolism. The sphingolipid and glycerophospholipid metabolic pathways were particularly affected. Additionally, in agreement with transcriptomic analyses, PS-NPs activate the hepatic TLR4/NF-κB pathway. At the same time, exposure to PS-NPs decreases the expression of ZO-1, occludin, and claudin-1, diminishes the relative abundance of beneficial gut bacteria (norank_f_Muribaculaceae, Akkermansia, and norank_f_norank_o_Clostridia_UCG-014), and increases the prevalence of pathogenic gut bacteria (Coriobacteriaceae_UCG-002 and Desulfovibrio), exacerbating liver injury through the gut-liver axis. However, administering DHA-PS (50 mg/kg) effectively alleviated these injuries.
This study was the first to employ multi-omics techniques to elucidate the potential mechanisms underlying hepatotoxicity induced by PS-NPs, thereby supporting the use of DHA-PS as a dietary supplement to mitigate the effects of nanoplastic pollutants.
塑料污染已成为一个不容忽视的全球性污染问题。作为人类口腔摄入的主要目的地,以肠道和肝脏为代表的塑料对消化系统的毒性作用是当前研究的焦点。海洋来源的 DHA-PS 具有多种生物活性,主要集中在改善大脑功能和调节脂质代谢上。然而,它是否对 PS-NPs 诱导的肝肠损伤有改善作用以及潜在的机制尚不清楚。
通过灌胃 PS-NPs 六周建立小鼠肝损伤模型。通过整合脂质组学、转录组学和肠道微生物组分析方法,通过“肠-肝轴”探讨 DHA-PS 缓解 PS-NPs 诱导的小鼠肝毒性的分子机制。
我们的研究结果表明,长期暴露于 PS-NPs 会导致显著的小鼠肝损伤和功能障碍,表现为氧化应激和炎症增加,以及肝脂质积累加剧。机制上,PS-NPs 通过抑制 SIRT1、AMPKα 和 PPARα 的表达,增强 SREBP-1c 的表达,从而破坏肝脏 SIRT1-AMPK 途径,最终导致肝脏脂质代谢紊乱。受影响的主要是鞘脂和甘油磷脂代谢途径。此外,与转录组分析结果一致,PS-NPs 激活了肝脏 TLR4/NF-κB 通路。同时,暴露于 PS-NPs 会降低 ZO-1、occludin 和 claudin-1 的表达,减少有益肠道细菌(norank_f_Muribaculaceae、Akkermansia 和 norank_f_norank_o_Clostridia_UCG-014)的相对丰度,并增加致病性肠道细菌(Coriobacteriaceae_UCG-002 和 Desulfovibrio)的流行率,通过肠-肝轴加重肝损伤。然而,给予 DHA-PS(50mg/kg)可有效缓解这些损伤。
本研究首次采用多组学技术阐明 PS-NPs 诱导肝毒性的潜在机制,支持将 DHA-PS 作为膳食补充剂用于减轻纳米塑料污染物的影响。