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Infected wound healing has always been a challenge in clinic. Effective and economic wound dressings with combined antibacterial activity and pro-healing function are highly desirable, especially in the context of infected wounds. An obvious advantage of antibacterial wound dressing is to avoid the overuse of antibiotics and the occurrence of drug resistance. Herein, an injectable hyaluronic acid hydrogel with antioxidative and photothermal antibacterial activity as a functional dressing was prepared, characterized and evaluated in an experimental infected wound model. This hydrogel was developed by loading graphene oxide (GO) in a natural polymer network consisting of hyaluronic acid grafted with tyramine (HT) and gelatin grafted with gallic acid (GGA). The HT/GGA/GO hydrogels have a porous cross-linked network structure and demonstrate a good stability, biocompatibility, antioxidant, hemostatic and photothermal antibacterial activity against Escherichia coli and Staphylococcus aureus. In addition, in vivo studies have shown that HT 1 /GGA 2 /GO 0.1 hydrogel dressing combined with photothermal therapy can effectively prevent early infection and accelerate wound healing. These results indicated this functionalized injectable hydrogel HT 1 /GGA 2 /GO 0.1 has a great potential in wound dressing application. [ABSTRACT FROM AUTHOR]

The incidence of cognitive impairment is rising globally, but there is no effective therapy. Recent studies showed that fucoidan (Fuc), a sulfated polysaccharide enriched in brown algae, is widely used due to its anti-inflammatory, antioxidant, and prebiotic effects. However, the effects and mechanisms of Fuc on lipopolysaccharide (LPS)-induced neuronal cell damage and cognitive impairment in mice need to be explored further. In the present study, we found that Fuc treatment protected HT22 cells from LPS-induced damage by inhibiting the activation of NLRP3 inflammasomes. Fuc exerted neuroprotective effects in mice with LPS-induced cognitive impairment by ameliorating neuroinflammation, promoting neurogenesis, and reducing blood-brain barrier and intestinal barrier permeability. Mechanistically, Fuc supplement significantly restructured the gut microbiota composition, which may be related to glucose and fructose metabolism. In conclusion, Fuc ameliorated LPS-induced neuronal cell damage and cognitive impairment in mice, suggesting that Fuc may be a medicinal and food homologous functional agent to improve cognitive function. The possible mechanism by which Fucoidan ameliorates LPS-induced cognitive impairment in mice, especially by remodeling gut microbiota. [Display omitted] • Fuc protected HT22 cells from LPS-induced damage via the inhibition of NLRP3 inflammasome. • Fuc exerted neuroprotective effects on LPS-induced cognitive impairment by reducing BBB and gut permeability. • Fuc remodeled the gut microbiota, which may be related to glucose and fructose metabolism. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a chronic neurodegenerative disease with high prevalence, long duration and poor prognosis. The blood-brain barrier (BBB) is a physiologic barrier in the central nervous system, which hinders the entry of most drugs into the brain from the blood, thus affecting the efficacy of drugs for AD. Natural products are recognized as one of the promising and unique therapeutic approaches to treat AD. To improve the efficiency and therapeutic effect of the drug across the BBB, a natural polyphenolic compound, procyanidin C-1 (C1) was encapsulated in glucose-functionalized bovine serum albumin (BSA) nanoparticles to construct Glu-BSA/C1 NPs in our study. Glu-BSA/C1 NPs exhibited good stability, slow release, biocompatibility and antioxidant properties. In addition, Glu-BSA/C1 NPs penetrated the BBB, accumulated in the brain by targeting Glut1, and maintained the BBB integrity both in vitro and in vivo. Moreover, Glu-BSA/C1 NPs alleviated memory impairment of 5 × FAD mice by reducing Aβ deposition and Tau phosphorylation and promoting neurogenesis. Mechanistically, Glu-BSA/C1 NPs significantly activated the PI3K/AKT pathway and inhibited the NLRP3/Caspase-1/IL-1β pathway thereby suppressing neuroinflammation. Taken together, Glu-BSA/C1 NPs could penetrate the BBB and mitigate neuroinflammation in AD, which provides a new therapeutic approach targeting AD. Schematic illustration of the synthesis and application of Glu-BSA/C1 NPs in a mouse model of Alzheimer's disease. [Display omitted] [ABSTRACT FROM AUTHOR]

The adverse microenvironment, including neuroinflammation, hinders the recovery of spinal cord injury (SCI). Regulating microglial polarization to alleviate neuroinflammation at the injury site is an effective strategy for SCI recovery. MG53 protein exerts obvious repair ability on multiple tissues damage, but with short half-life. In this study, we composited an innovative MG53/GMs/HA-Dex neural scaffold using gelatin microspheres (GMs), hyaluronic acid (HA), and dextran (Dex) loaded with MG53 protein. This novel neural scaffold could respond to MMP-2/9 protein and stably release MG53 protein with good physicochemical properties and biocompatibility. In addition, it significantly improved the motor function of SCI mice, suppressed M1 polarization of microglia and neuroinflammation, and promoted neurogenesis and axon regeneration. Further mechanistic experiments demonstrated that MG53/GMs/HA-Dex hydrogel inhibited the JAK2/STAT3 signaling pathway. Thus, this MG53/GMs/HA-Dex neural scaffold promotes the functional recovery of SCI mice by alleviating neuroinflammation, which provides a new intervention strategy for the neural regeneration and functional repair of SCI. Schematic illustration of the preparation and application of MG53/GMs/HA-Dex neural scaffolds in a mouse model of spinal cord injury. [Display omitted] • MGHD responded to MMP-2/9 and stably released MG53 protein with good physicochemical properties and biocompatibility. • MGHD improved the motor function of SCI mice, suppressed neuroinflammation, and promoted neurogenesis and axon regeneration. • MGHD inhibited the JAK2/STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is one of the most devastating nervous injuries. Neural tissue engineering based on stem cells and bioactive scaffold is a promising but challenging approach for neural repair. A cutting-edge system with capability to control the fate of encapsulated stem cells is attractive to enhance neural regeneration after TBI. Herein, an injectable gelatin hydrogel dual-enzymatically cross-linked by horse radish peroxidase (HRP) and choline oxidase (ChOx) was performed as the neural scaffold to load murine bone marrow-derived mesenchymal stem cells (BMSC) for TBI treatment. The results of in vitro cellular experiments showed that low cross-linked gelatin hydrogel could obviously promote cellular viability, neural differentiation, and neurotrophins secretion of the loaded BMSC. In vivo tests on a TBI model of C57BL/6 mouse demonstrated that BMSC-laden gelatin hydrogel implants could significantly reduce the damaged area, ameliorate inflammation, attenuate neuronal apoptosis, facilitate survival and proliferation of endogenous neural cells, and promote the neurological function recovery of TBI mice. All data suggest that establishment of this three-dimensional (3D) gelatin hydrogel stem cell-loaded system is a promising therapeutic strategy for TBI or other neurological rehabilitation. [Display omitted] • An injectable and dual-enzymatically cross-linked gelatin hydrogel was used to load BMSC for TBI treatment • Low cross-linked gelatin hydrogel obviously enhances cellular viability, neural differentiation, and neurotrophin secretion • This GH/MSC hydrogel implantation could promote the neurogenesis and functional reconstruction of TBI mice [ABSTRACT FROM AUTHOR]