Abstract

Selenium (Se) as an essential micronutrient plays a crucial role in human health. Biogenic selenium nanoparticles (SeNPs) possess attractive biological properties, biocompatibility, stability and low-toxicity. This study was aimed to investigate the protective effect of biogenic SeNPs of size 50-80 nm synthesized by Lactobacillus casei ATCC 393 (L. casei ATCC 393) on diquat-induced intestinal barrier dysfunction in C57BL/6 mice and the intrinsic mechanisms. Our results showed that oral administration of SeNPs significantly inhibited the increase of the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), diamine oxidase (DAO) and d-lactic acid (d-LA) levels induced by diquat, and increased the total superoxide dismutase (T-SOD), thioredoxin reductase (TrxR) and glutathione peroxidase (GSH-Px) activities in serum and jejunum. Moreover, SeNPs increased the number of goblet cells, decreased the production of reactive oxygen species (ROS), maintained the mitochondrial functions, and improved the expression levels of occludin and claudin-1 in jejunum compared to the diquat-induced oxidative stress model group. In addition, SeNPs activated the nuclear factor (erythroid-derived-2)-like 2 (Nrf2), and improved the protein levels of heme oxygenase (HO)-1 and NADPH dehydrogenase (NQO)-1 compared to other treatment groups. These results suggested that biogenic SeNPs synthesized by L. casei ATCC 393 can protect the intestinal barrier function against oxidative damage via Nrf2-mediated signaling pathway.

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