Biofouling causes numerous adverse impacts on devices and instruments in a marine environment. The main purpose of the present study is to develop a bioinspired and ecofriendly coating for inhibiting marine biofouling. Herein, based on a bacteriostatic and bactericidal synergistic method, we reported a selfadhesive lubricating copolymer with functional pendant groups, which was synthesized by free radical polymerization using dopamine methacrylamide (DMA), 2-methacryloyloxyethyl phosphorylcholine (MPC), and N-methacryloyloxy benzoisothiazolinone (M-BIT). The copolymer could self-adhere on the steel sheet with a simple dip-coating method and formed an effective antifouling coating on the surface. The adhesion behavior and lubrication property of the copolymer were investigated using X-ray photoelectron spectroscopy and atomic force microscopy. The antibacterial test demonstrated that the copolymer was efficient in inhibiting the accumulation of bacterial biofilm and normal growth of E. coli and S. aureus, and the algae inhibition test revealed that the copolymer had great suppression ability against Chlorella and Nitzschia closterium. Furthermore, the marine field test showed that the copolymer was endowed with excellent antifouling property, which was owing to the bacteriostatic performance of zwitterionic phosphocholine groups in MPC and the bactericidal effect of M-BIT. In conclusion, the bioinspired copolymer can achieve effective marine biofouling prevention by a bactericidal and bacteriostatic synergistic strategy, and it may be used as a self-adhesive coating for achieving surface functionalization of marine devices and instruments.

Background Neuroinflammatory response is considered to be a high-risk factor for cognitive impairments in the brain. Lipopolysaccharides (LPS) is an endotoxin that induces acute inflammatory responses in injected bodies. However, the molecular mechanisms underlying LPS-associated cognitive impairments still remain unclear. Methods Here, primary hippocampal neurons were treated with LPS, and western blotting and immunofluorescence were used to investigate whether LPS induces neurons damage. At the same time, SD rats were injected with LPS (830 μg/Kg) intraperitoneally, and Open field test, Novel Objective Recognition test, Fear condition test were used to detect cognitive function. LTP was used to assess synaptic plasticity, and molecular biology technology was used to assess the NF-κB pathway, while ELISA was used to detect inflammatory factors. In addition, metformin was used to treat primary hippocampal neurons, and intraventricularly administered to SD rats. The same molecular technics, behavioral and electrophysiological tests were used to examine whether metformin could alleviate the LPS-associated neuronal damage, as well as synaptic plasticity, and behavioral alterations in SD rats. Results Altogether, neuronal damage were observed in primary hippocampal neurons after LPS intervention, which were alleviated by metformin treatment. At the same time, LPS injection in rat triggers cognitive impairment through activation of NF-κB signaling pathway, and metformin administration alleviates the LPS-induced memory dysfunction and improves synaptic plasticity. Conclusion These findings highlight a novel pathogenic mechanism of LPS-related cognitive impairments through activation of NF-κB signaling pathway, and accumulation of inflammatory mediators, which induces neuronal pathologic changes and cognitive impairments. However, metformin attenuates LPS-induced neuronal injury and cognitive impairments by blocking NF-κB pathway.

Background Sepsis is considered to be a high-risk factor for cognitive impairment in the brain. The purpose of our study is to explore whether sepsis causes cognitive impairment and try to evaluate the underlying mechanisms and intervention measures. Methods Here, we used cecum ligation and puncture (CLP) to simulate sepsis. Open field, Novel Objective Recognition, and Morris Water Maze Test were used to detect cognitive function, long-term potentiation was used to assess of synaptic plasticity, and molecular biological technics were used to assess synaptic proteins, ELISA kits were used to detect inflammatory factors. Metformin was injected into the lateral ventricle of SD rats, and we evaluated whether metformin alleviated CLP-mediated cognitive impairment using behavioral, electrophysiological and molecular biological technology experiments. Results Here we report hippocampal-dependent cognitive deficits and synaptic dysfunction induced by the CLP, accompanied by a significant increase in inflammatory factors. At the same time, metformin was able to improve cognitive impairment induced by CLP in adult male rats. Conclusion These findings highlight a novel pathogenic mechanism of sepsis-related cognitive impairment through activation of inflammatory factors, and these are blocked by metformin to attenuate sepsis-induced neuronal injury and cognitive impairment.