Effects of adding lignocellulose-degrading microbial agents and biochar on nitrogen metabolism and microbial community succession during pig manure composting.

This study assessed the influence of the additions of lignocellulose-degrading microbial agents and biochar on nitrogen (N) metabolism and microbial community succession during pig manure composting. Four treatments were established: CK (without additives), M (lignocellulose-degrading microbial agents), BC (biochar), and MBC (lignocellulose-degrading microbial agents and biochar). The results revealed that all treatments with additives decreased N loss compared with CK. In particular, the concentrations of total N and NO3--N were the highest in M, which were 21.87% and 188.67% higher than CK, respectively. Meanwhile, the abundance of denitrifying bacteria Flavobacterium, Enterobacter, and Devosia reduced with additives. The roles of Anseongella (nitrifying bacterium) and Nitrosomonas (ammonia-oxidizing bacterium) in NO3--N transformation were enhanced in M and BC, respectively. N metabolism pathway prediction indicated that lignocellulose-degrading microbial agents addition could enhance N retention effectively mainly by inhibiting denitrification. The addition of biochar enhanced oxidation of NH4+-N to NO2--N and N fixation, as well as inhibited denitrification. These results revealed that the addition of lignocellulose-degrading microbial agents individually was more conducive to improve N retention in pig manure compost.

Metformin attenuates sepsis-induced neuronal injury and cognitive impairment.

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.

Metformin attenuates LPS-induced neuronal injury and cognitive impairments by blocking NF-κB pathway.

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.