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Background: Acute liver failure (ALF) is a severe liver disease with high morbidity and mortality rates. Animal models are important for research on ALF. This study aimed to establish a reproducible, Tibetan miniature pig model of D-galactosamine-induced ALF and verify it using a dual plasma molecular adsorption system (DPMAS).Methods: Tibet miniature pigs were randomly divided into four groups (A, B, C, D) after catheterization. D-galactosamine (D-gal) at 0.45, 0.40, 0.35, and 0.35 g/kg body weight, respectively, was injected through the catheter. Group D was treated with DPMAS 48 h after D-gal administration. Vital signs and blood index values were recorded every 12 h after D-gal administration. H&E, TUNEL, Ki67, and Masson staining tests were performed.Results: After D-gal administration, Tibetan miniature pigs developed different degrees of debilitation, loss of appetite, and jaundice. Survival times of groups A, B, C, and D were 39.7 ± 5.9, 53.0 ± 12.5,61.3 ± 8.1, and 61 ± 7 h, respectively. Blood levels of ALT, AST, TBIL, ammonia, PT, and inflammation factors significantly increased compared with baseline levels in the different groups (Ps < 0.05). Pathological results revealed a clear liver cell necrosis positive correlation with D-gal dose. However, DPMAS did not increase the survival time in ALF, ammonia, or liver cell necrosis.Conclusion: We successfully established a reproducible Tibetan miniature pig model of d-galactosamine-induced ALF, and we believe that a dosage of 0.35 g/kg is optimal.

Staphylococcus aureus(S. aureus) can survive phagocytosis and gain shelter from macrophages in some cases, and the clinical treatment of the intracellular bacterium also encounters the difficulty of traditional antibiotics in entering mammalian cells. In this work, we use mannose-modified bioactive glass nanoparticles decorated with silver nanoparticles (BGNs-Man/Ag) to treat the S. aureus-induced intracellular infection of macrophages. The results showed that BGNs-Man/Ag could target macrophages, elevate the intracellular ROS levels and drive them toward the M1 phenotype, which was crucial to activate the cell autonomous defence in disposing the intracellular infection. Attractively, BGNs-Man/Ag exhibited higher intracellular bacterial killing efficiency than free vancomycin. For the in vivotreatment of subcutaneous abscess, BGNs-Man/Ag significantly increased the population of M1 macrophages at the early stages of the infection site, resulting in enhanced bactericidal activity and improved regeneration of skin tissues. In short, BGNs-Man/Ag can be a promising antibacterial material in treating the S. aureus-induced intracellular infection of macrophages and subcutaneous abscesses.