ABSTRACT
Acetaminophen (APAP)-induced liver injury (AILI) is a pressing public health concern. Although evidence suggests that Bifidobacterium adolescentis (B. adolescentis) can be used to treat liver disease, it is unclear if it can prevent AILI. In this report, we prove that B. adolescentis significantly attenuated AILI in mice, as demonstrated through biochemical analysis, histopathology, and enzyme-linked immunosorbent assays. Based on untargeted metabolomics and in vitro cultures, we found that B. adolescentis generates microbial metabolite hypaphorine. Functionally, hypaphorine inhibits the inflammatory response and hepatic oxidative stress to alleviate AILI in mice. Transcriptomic analysis indicates that Cry1 expression is increased in APAP-treated mice after hypaphorine treatment. Overexpression of Cry1 by its stabilizer KL001 effectively mitigates liver damage arising from oxidative stress in APAP-treated mice. Using the gene expression omnibus (GEO) database, we verified that Cry1 gene expression was also decreased in patients with APAP-induced acute liver failure. In conclusion, this study demonstrates that B. adolescentis inhibits APAP-induced liver injury by generating hypaphorine, which subsequently upregulates Cry1 to decrease inflammation and oxidative stress.
Subject(s)
Acetaminophen , Bifidobacterium adolescentis , Chemical and Drug Induced Liver Injury , Liver , Mice, Inbred C57BL , Animals , Acetaminophen/adverse effects , Chemical and Drug Induced Liver Injury/metabolism , Chemical and Drug Induced Liver Injury/pathology , Liver/drug effects , Liver/pathology , Liver/metabolism , Male , Humans , Oxidative Stress/drug effects , Mice , Gene Expression Regulation/drug effects , PyridinesABSTRACT
Preserving the integrity of carbon fibers when recycling carbon-fiber-reinforced plastics (CFRPs) has been unfeasible due to the harsh reaction conditions required to remove epoxy resin matrixes, which adversely affect the properties of carbon fibers. We establish a practicable and environmentally friendly reclamation strategy for carbon fibers. Carbon fibers are recycled from waste CFRPs by an electrochemical catalytic reaction with the assistance of phosphotungstic acid (PA), which promotes the depolymerization of diglycidyl ether of bisphenol A/ethylenediamine (DGEBA/EDA) epoxy resin. The removal rate, mechanical strength, and microstructure of the recycled carbon fibers are analyzed to explore the mechanism of the electrochemical treatment. The influence of three factors-current density, PA concentration, and reaction time-are studied via an orthogonal method. Range analysis and variance analysis are conducted to investigate the significance of the factors. The optimal conditions are determined accordingly. The underlying CFRP degradation mechanism is also investigated.
