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Abstract Objective This study aims to investigate the biocompatibility and pharmacokinetic characteristics of polyvinyl pyrrolidone-modified selenium nanoparticles (PVP-Se NPs). Understanding the biosafety of PVP-Se NPs is crucial due to their potential applications in mitigating oxidative stress-related diseases and improving drug delivery systems. Methods Selenium nanoparticles were prepared using a sodium selenite solution, followed by PVP modification. Particle size analysis was conducted using dynamic light scattering (DLS), and particle morphology was observed using transmission electron microscopy (TEM). Different concentrations of PVP-Se NPs were intraperitoneally injected into SD rats, and the survival rate was observed. Liver and kidney tissues, urine, feces, and blood samples were collected at the highest safe dose, and the concentration of selenium ions was measured. Results The average particle size of PVP-Se NPs was 278.4 ± 124.8 nm, exhibiting a semi-spherical shape. The maximum safe dose of PVP-Se NPs for intraperitoneal injection in rats was approximately 320 µg/kg. At this dose, the content of PVP-Se NPs significantly increased in the liver and kidney tissues from day 1 to day 3, in urine and feces during the first 8 h, and in blood during the first 2 h, followed by a gradual decrease. Conclusion When administered at a safe dose, PVP-Se NPs do not damage liver and kidney tissues and can be eliminated from the body through liver and kidney metabolism without accumulation.

Abstract According to numerous reports, Trichinella spiralis (T. spiralis) and its antigens can reduce intestinal inflammation by modulating regulatory immunological responses in the host to maintain immune homeostasis. Galectin has been identified as a protein that is produced by T. spiralis, and its characterization revealed this protein has possible immune regulatory activity. However, whether recombinant T. spiralis galectin (rTs-gal) can cure dextran sulfate sodium (DSS)-induced colitis remains unknown. Here, the ability of rTs-gal to ameliorate experimental colitis in mice with inflammatory bowel disease (IBD) as well as the potential underlying mechanism were investigated. The disease activity index (DAI), colon shortening, inflammatory cell infiltration, and histological damage were used as indicators to monitor clinical symptoms of colitis. The results revealed that the administration of rTs-gal ameliorated these symptoms. According to Western blotting and ELISA results, rTs-gal may suppress the excessive inflammatory response-mediated induction of TLR4, MyD88, and NF-κB expression in the colon. Mice with colitis exhibit disruptions in the gut flora, including an increase in gram-negative bacteria, which in turn can result in increased lipopolysaccharide (LPS) production. However, injection of rTs-gal may inhibit changes in the gut microbiota, for example, by reducing the prevalence of Helicobacter and Bacteroides, which produce LPS. The findings of the present study revealed that rTs-gal may inhibit signalling pathways that involve enteric bacteria-derived LPS, TLR4, and NF-κB in mice with DSS-induced colitis and attenuate DSS-induced colitis in animals by modulating the gut microbiota. These findings shed additional light on the immunological processes underlying the beneficial effects of helminth-derived proteins in medicine.