Abstract：
Dietary pollution by polystyrene microplastics (MPs) can cause hepatic injuries and microbial dysbiosis. Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, exerts beneficial effects on the liver by modulating the gut microbiota. However, the role of microbiota in MPs-induced hepatic injuries and the protective effect of EGCG have not been clarified. Here, 5 μm MPs were orally administered to mice to induce hepatic injuries. Subsequently, antibiotic cocktail (ABX) and fecal microbial transplant (FMT) experiments were performed to investigate the underlying microbial mechanisms. Additionally, EGCG was orally administered to mice to explore its protection against MPs-induced hepatic injuries. Our results showed that MPs activated systemic and hepatic inflammation, promoted fibrosis, and altered the liver metabolome; meanwhile, MPs damaged the gut homeostasis by disturbing the gut microbiome, promoting colonic inflammation, and impairing the intestinal barrier. Notably, MPs reduced the abundance of the probiotics Akkermansia, Mucispirillum, and Faecalibaculum while increasing the pathogenic Tuzzerella. Interestingly, the elimination of gut microbiota mitigated MPs-induced colonic inflammation and intestinal barrier impairment. Moreover, ABX ameliorated MPs-induced systemic and hepatic inflammation but not fibrosis. Correspondingly, microbiota from MPs-administered mice induced colonic, systemic, and hepatic inflammation, while their profibrosis effect on the liver was not observed. Finally, EGCG elevated the abundance of probiotics and effectively repressed MPs-induced colonic inflammation. MPs-induced systemic and hepatic inflammation, fibrosis, and remodeling of the liver metabolome were also attenuated by EGCG. These findings illustrated that gut microbiota contributed to MPs-induced colonic and hepatic injuries, while EGCG could serve as a potential prevention strategy for these adverse consequences.
摘要：
聚苯乙烯微塑料（MPs）的饮食污染可导致肝损伤和微生物菌群失调。表没食子儿茶素-3-没食子酸酯（EGCG），绿茶中的主要多酚，通过调节肠道菌群对肝脏产生有益作用。然而,微生物群在MPs诱导的肝损伤中的作用以及EGCG的保护作用尚未阐明.这里,将5μmMPs口服给予小鼠以诱导肝损伤。随后，进行了抗生素混合物(ABX)和粪便微生物移植(FMT)实验,以研究潜在的微生物机制.此外,给小鼠口服EGCG以探索其对MPs诱导的肝损伤的保护作用。我们的结果表明，MPs激活全身和肝脏炎症，促进纤维化，并改变了肝脏代谢组；同时，国会议员通过扰乱肠道微生物群来破坏肠道稳态，促进结肠炎症，并损害肠道屏障。值得注意的是,MPs减少了益生菌Akkermansia的丰度，Mucispirillum,和粪杆菌，同时增加致病性油菌。有趣的是,肠道菌群的消除减轻了MPs诱导的结肠炎症和肠屏障损伤.此外，ABX改善MPs诱导的全身和肝脏炎症，但不改善纤维化。相应地,来自施用MPs的小鼠诱导的结肠微生物群，系统性，和肝脏炎症，而未观察到它们对肝脏的促纤维化作用。最后,EGCG提高了益生菌的丰度并有效抑制了MPs诱导的结肠炎症。MPs诱导的全身和肝脏炎症，纤维化，EGCG也减弱了肝脏代谢组的重塑。这些研究结果表明，肠道微生物群有助于MPs诱导的结肠和肝损伤，而EGCG可以作为这些不良后果的潜在预防策略。
