Search

In this work, a magnetic CoFe alloy and Co supported on mesoporous carbon with abundant defects (CoFe–Co/MC) was prepared by a sol–gel method combined with calcination and applied to activate peroxymonosulfate (PMS) and efficiently remove bensulfuron methyl (BSM) from water. CoFe–Co/MC could degrade 95% of BSM, while Co or Fe without supported mesoporous carbon could only provide degradation efficiencies below 10%, indicating that the introduction of mesoporous carbon could effectively enhance catalytic activity. Moreover, the dissolution of Co2+ from CoFe–Co/MC is only 0.22 mg L−1, which is about 20% of Co/MC, indicating that the bimetallic composite effectively inhibits the dissolution. The results of radical scavenger and EPR experiments demonstrated that 1O2 played the leading role in degradation process, while SO4˙− and small amounts of ˙OH and O2˙− were also involved in the degradation. The results of p-BQ scavenger and N2 atmosphere experiments showed that 1O2 mainly originated from the interaction between carbon defects and dissolved oxygen. The degradation performance of the CoFe–Co/MC/PMS system, carbon defect content and 1O2 content all increased with the increase of pyrolysis temperature, which demonstrated that adjusting pyrolysis temperature can regulate carbon defect content and 1O2 content, further improving catalytic activity. Possible BSM degradation pathways of CoFe–Co/MC/PMS were investigated in detail. This research provides new insights into the design and construction of metal–carbon catalysts rich in carbon defects and reveals how to regulate carbon defect content, 1O2 content and catalytic performance. [ABSTRACT FROM AUTHOR]

Background: Huanshaodan (HSD) is a Chinese Herbal Compound which has a definite clinical effect on Alzheimer's disease (AD), however, the underlying mechanism remains unclear. The aim of this study is to preliminarily reveal the mechanism of HSD in the treatment of AD model of SAMP8 mice. Methods: Chemical composition of HSD and its drug-containing serum were identified by Q-Orbitrap high resolution liquid mass spectrometry. Six-month-old SAMP8 mice were treated with HSD and Donepezil hydrochloride by gavage for 2 months, and Wogonin for 28 days. Behavioral test was performed to test the learning and memory ability of mice. Immunofluorescence (IF) or Western-blot methods were used to detect the levels of pSer404-tau and β-amyloid (Aβ) in the brain of mice. Hematoxylin–eosin (H&E) staining and Transmission electron microscopy (TEM) assay was applied to observe the pathological changes of neurons. Proteomic technology was carried out to analyze and identify the protein network of HSD interventions in AD. Then the pathological process of the revealed AD-related differential proteins was investigated by IF, Q-PCR, Western-blot, Fluorescence in situ hybridization (FISH) and 16S rRNA sequencing methods. Results: The results showed that HSD and Wogonin, one of the components in its drug-containing serum, can effectively improve the cognitive impairments of SAMP8 mice, protect hippocampal neurons and synapses, and reduce the expression of pSer404-tau and Aβ. HSD and Wogonin reduced the levels of fibrinogen β chain (FGB) and γ chain (FGG), the potential therapeutic targets revealed by proteomics analysis, reduced the colocalization of FGB and FGG with Aβ, ionized calcium binding adaptor molecule 1 (Iba-1), glial fibrillary acidic protein (GFAP), increased level of and myelin basic protein (MBP). Meanwhile, HSD and Wogonin increased ZO-1 and Occludin levels, improved brain microvascular injury, and reduced levels of bacteria/bacterial DNA and lipopolysaccharide (LPS) in the brain of mice. In addition, 16S rRNA sequencing indicated that HSD regulated the structure of intestinal microbiota of mice. Conclusion: The effects of HSD on AD may be achieved by inhibiting the levels of fibrinogen and the interactions on glia cells in the brain, and by modulating the structure of intestinal microbiota and improving the blood–brain barrier function. [ABSTRACT FROM AUTHOR]

This study aims to investigate the relevant mechanism by which hydrazinocurcumin (HC) interferes with A431 cell autophagy by inhibiting the STAT3 signaling pathway. Different concentrations of HC are used to treat A431 cells to study the effects of HC on A431 cell proliferation and apoptosis. Real‐time fluorescent quantitative polymerase chain reaction (PCR) is used to further explore the relationship of HC with the JAK signaling pathway and autophagy. Double immunofluorescence staining is used to detect the fluorescence localization of LC3 and STAT3 after HC treatment. With increasing HC concentrations, A431 cell viability decreases in a dose‐dependent manner, and the apoptosis rate increases significantly. Laser confocal colocalization reveals that the fluorescence of labeled LC3 protein is significantly increased, and the fluorescence of labeled STAT3 is significantly reduced in this study. HC may induce autophagy in A431 cells and affect cell proliferation by downregulating the JAK/STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

In this study, rice straw biochar modified with Co3O4-Fe3O4 (RSBC@Co3O4-Fe3O4) was successfully prepared via calcinating oxalate coprecipitation precursor and employed as a catalyst to activate peroxymonosulfate (PMS) for the treatment of Rhodamine B (RhB)-simulated wastewater. The results indicated that RSBC@Co3O4-Fe3O4 exhibited high catalytic performance due to the synergy between Co3O4 and Fe3O4 doping into RSBC. Approximately 98% of RhB (180 mg/L) was degraded in the RSBC@Co3O4-Fe3O4/PMS system at initial pH 7 within 15 min. The degradation efficiency of RhB maintained over 90% after the fourth cycle, illustrating that RSBC@Co3O4-Fe3O4 displayed excellent stability and reusability. The primary reactive oxygen species (ROS) answerable for the degradation of RhB were 1O2, •OH, and SO4•−. Moreover, the intermediates involved in the degradation of RhB were identified and the possible degradation pathways were deduced. This work can provide a new approach to explore Co-based and BC-based catalysts for the degradation of organic pollutants. [ABSTRACT FROM AUTHOR]