Hao Yuan,Xiaoxue Han,Zhizheng Sheng,Jian Zhou,Zhendong Wang,Yingchun Ye,Yongfeng Hu,Weimin Yang
Zeolites have been widely employed in industrial catalysis, but the application of zeolites was often limited by their hydrothermal stability. As a successfully applied method for enhancing hydrothermal stability of zeolites, phosphorus (P) modification has been faced with issues such as polymerization and low utilization of P precursor. In this work, we developed a strategy for the P modification of zeolites via trimethylphosphine oxide (TMPO) selective adsorption. Thanks to its alkaline property, TMPO could be adsorbed selectively on the acid sites of zeolites and maintains strong interaction with framework aluminum during further redistribution and oxidation treatments. Extensive characterizations, such as 27Al and 31P MAS NMR, pyridine-FTIR, and P K-edge XANES, were employed to study the transformation of P–Al interaction in zeolites during hydrothermal treatment. It was revealed that the P species adsorbed on strong acid sites were beneficial to the production of a stronger P–Al interaction. Hydrothermal experimental results proved that the P-modified zeolites with a stronger P–Al interaction exhibited higher retention of Bro̷nsted acid sites, resulting from the greatly reduced polymerization of P to protect more framework aluminum. Our approach demonstrates the potential of TMPO modification in controlling P–Al interaction to enhance the hydrothermal stability of zeolites for the methanol to hydrocarbon reaction.
ABSTRACT Epicatechin (EC) has significant antiinflammation, antioxidation, and anticancer activities. It also provides a new alternative treatment for mastitis, which can result in great economic losses in the dairy industry if left untreated. The purpose of this study was to investigate the anti-inflammatory effects of EC on mastitis and the underlying mechanism using in vivo and in vitro systems. The use of ELISA and immunohistochemistry assays showed that EC treatment at 1.5, 7.5, 15, and 30 mg/mL decreased protein expression of inflammatory mediators, including cyclooxygenase-2 and inducible nitric oxide synthase; inflammatory cytokines, which were composed of IL-1β, TNF-α, and IL-6 in lipopolysaccharide (LPS)-stimulated bovine mammary epithelial cell line (MAC-T); and mouse mammary gland, together with reduced filtration of T lymphocytes in the mouse mammary gland. Furthermore, EC treatment reduced LPS-induced phosphorylation levels of p65 and inhibitor of NF-κB, and blocked nuclear translocation of p65 as revealed by western blot and immunofluorescence test in MAC-T cells and the mouse mammary gland. Epicatechin also attenuated LPS-induced phosphorylation levels of mitogen-activated protein kinase members (i.e., p38, c-Jun N-terminal kinase 1/2 and extracellular regulated protein kinases 1/2). Using RNA-seq and tandem mass tag analyses, upregulation of TMEM35A and TMPO proteins was disclosed in MAC-T cells cotreated with LPS and EC. Although clustered regularly interspaced short palindromic repeats/Cas9-based knockdown of TMEM35A and TMPO attenuated abundance of phosphorylated (p)-p65, p-p38, TNF-α, and iNOS, overexpression of TMEM35A reversed EC-mediated effects in TMPO knockdown cells. Moreover, interaction between TMEM35A and TMPO was detected using the co-immunoprecipitation method. In conclusion, our data demonstrated that EC inhibited LPS-induced inflammatory response in MAC-T cells and the mouse mammary gland. Importantly, TMEM35A mediated the transmembrane transport of EC, and the interaction between TMEM35A and TMPO inhibited MAPK and NF-κB pathways.
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