Abstract

Nanoplastics and food-grade nanoparticles are increasingly recognised as potential environmental factors that can lead to metabolic dysfunction. However, their effects under vulnerable metabolic conditions and the potential role of probiotics are still insufficiently understood. The aim of this study was to investigate whether silicon nanoparticles (SiNPs) exacerbate fructose-induced intestinal damage associated with metabolic syndrome (MetS), and to evaluate the protective effects of Lactiplantibacillus plantarum P101 ( L . plantarum P101), particularly its role in regulating the gut microbiota. A fructose-fed mouse model combined with chronic oral SiNPs exposure was established, followed by intervention with L. plantarum P101. Metabolic parameters, intestinal histopathology, inflammatory responses, oxidative stress-related signaling, intestinal barrier integrity, gut microbiota composition, and fecal microbiota transplantation (FMT) were analyzed. SiNPs aggravated fructose-induced metabolic abnormalities and intestinal injury, accompanied by impaired barrier-related responses, enhanced inflammation, altered oxidative stress signalling, and gut microbiota dysbiosis. L. plantarum P101 alleviated these alterations, accompanied by improved intestinal barrier-related markers, reduced inflammatory responses, and modulation of gut microbial composition. Specifically, Lactobacillus - and Bifidobacterium -related taxa were enriched, whereas inflammation-associated bacterial groups were reduced. FMT experiments corroborated the association between gut microbiota alterations and the protective phenotype, suggesting that microbial factors may contribute to the observed benefits. Overall, these findings suggest that SiNPs may amplify metabolic and intestinal dysfunction under susceptible conditions, while L. plantarum P101 provides protective effects associated with improved barrier responses, reduced inflammation, and gut microbiota modulation.