Achilles tendon is a motor organ that is prone to tissue adhesion during its repair process after rupture. Therefore, developing motion-responsive and anti-adhesive biomaterials is an important need for the repair of Achilles tendon rupture. Here, we report an injectable lubricative hydrogel (ILH) based on hydration lubrication mechanism, which is also motion-responsive based on sol-gel reversible transmission. The lubrication performance is achieved by zwitterionic polymers as we previously proved, and the sol-gel reversible transmission is enabled by dynamic disulfide bonds. Firstly, ILH was proved to be successfully prepared and lubricated as well as sol-gel reversible via FTIR characterization, rheological measurement and tribological tests. Then, in vitro cell experiments and coagulation tests demonstrated the optimal cytocompatibility and hemocompatibility of ILH. To evaluate the potential of ILH's biofunction in vivo, SD rats' Achilles tendon rupture & repair model was established. The animal experiments' results showed that ILH significantly prevented tendon adhesion and thus promote tendon healing by inhibiting TGFβ1-Smad2/3 pathway. We believe this work will open a new horizon for tendon adhesion-free repair.

Tissue infection typically results from blood transmission or the direct inoculation of bacteria following trauma. The pathogen-induced destruction of tissue prevents antibiotics from penetrating the infected site, and severe inflammation further impairs the efficacy of conventional treatment. The current study describes the size-dependent induction of macrophage polarization using gold nanoparticles. Gold nanoparticles with a diameter of 50 ​nm (Au50) can induce M2 polarization in macrophages by inhibiting the NF-κB signaling pathway and stimulate an inflammatory response in the environment by inhibiting the MAPK signaling pathway LPS. Furthermore, the induced polarization and anti-inflammatory effects of the Au50 nanoparticles promoted the osteogenic differentiation of BMSCs in vitro. In addition, the overexpression of TREM2 in macrophage induced by Au50 nanoparticles was found to promote macrophage phagocytosis of Staphylococcus aureus, enhance the fusion of autophagosomes and lysosomes, accelerate the intracellular degradation of S. aureus, in addition to achieving an effective local treatment of osteomyelitis and infectious skin defects in conjunction with inflammatory regulation and accelerating bone regeneration. The findings, therefore, demonstrate that Au50 nanoparticles can be utilized as a promising nanomaterial for in vivo treatment of infections.

Background: Inhibiting ROS overproduction is considered a very effective strategy for the treatment of peripheral nerve injuries, and Se has a remarkable antioxidant effect; however, since the difference between the effective concentration of Se and the toxic dose is not large, we synthesized a nanomaterial that can release Se slowly so that it can be used more effectively. Methods: Se@SiO₂ NPs were synthesized using a mixture of Cu_2-x Se nanocrystals, and the mechanism of action of Se@SiO₂ NPs was initially explored by performing sequencing, immunofluorescence staining and Western blotting of cellular experiments. The mechanism of action of Se@SiO₂ NPs was further determined by performing behavioral assays after animal experiments and by sampling the material for histological staining, immunofluorescence staining, and ELISA. The effects, mechanisms and biocompatibility of Se@SiO₂ NPs for peripheral nerve regeneration were determined. Results: Porous Se@SiO₂ was successfully synthesized, had good particle properties, and could release Se slowly. CCK-8 experiments revealed that the optimal experimental doses were 100 μM H₂O₂ and 200 μg/mL Se@SiO₂, and RNA-seq revealed that porous Se@SiO₂ was associated with cell proliferation, apoptosis, and the PI3K/AKT pathway. WB showed that porous Se@SiO₂ could increase the expression of cell proliferation antigens (PCNA and S100) and antiapoptotic proteins (Bcl-2), decrease the expression of proapoptotic proteins (Bax), and increase the expression of antioxidative stress proteins (Nrf2, HO-1, and SOD2). EdU cell proliferation and ROS fluorescence assays showed that porous Se@SiO2 promoted cell proliferation and reduced ROS levels. The therapeutic effect of LY294002 (a PI3K/AKT pathway inhibitor) was decreased significantly and its effect was lost when it was added simultaneously with porous Se@SiO₂. Animal experiments revealed that the regenerated nerve fiber density, myelin thickness, axon area, gastrocnemius muscle wet-to-weight ratio, myofiber area, sciatic nerve function index (SFI), CMAP, apoptotic cell ratio, and levels of antioxidative stress proteins and anti-inflammatory factors were increased following the administration of porous Se@SiO₂. The levels of oxidative stress proteins and anti-inflammatory factors were significantly greater in the Se@SiO₂ group than in the PNI group, and the effect of LY294002 was decreased significantly and was lost when it was added simultaneously with porous Se@SiO₂. Conclusion: Se@SiO₂ NPs are promising, economical and effective Se-releasing nanomaterials that can effectively reduce ROS production, inhibit apoptosis and promote cell proliferation after nerve injury via the PI3K/AKT pathway, ultimately accelerating nerve regeneration. These findings could be used to design new, promising drugs for the treatment of peripheral nerve injury.