No abstract

Stearic acid (SA) and hexadecanamide (HA), which are model compounds of algae-based bio-oil, were used to produce aromatics for catalysis by a hierarchical HZSM-5 zeolite under hydrothermal conditions. The results showed that the hierarchical HZSM-5 zeolite was more active than the traditional HZSM-5 parent zeolite. The molar yield of toluene, ethylbenzene, and xylene could reach (1.14 ± 0.05) × 100% (normal weight percentage yield = 40.77 wt %) when the reaction temperature was 400 °C. Moreover, the catalyst was stable and recyclable under hydrothermal conditions. Besides, the addition of acetic acid remarkably improved the deoxygenation (or denitrification) and aromatization efficiencies of the SA and HA mixture by more than 25%. This study provides a feasible approach to the valorization of algal biomass and the production of aromatics.

No abstract

Atherosclerosis is a lipid-driven chronic inflammatory disease in which lipid-laden macrophage foam cells lead to inflamed lesions in arteries. Previous studies have proven that sulfotransferase 2B1b (SULT2B1b) has several roles in the regulation of lipid metabolism and the inflammatory response. However, little is known about the functions of SULT2B1b in ox-LDL-induced inflammation in macrophages. In this study, after treatment with either ox-LDL alone or combined with transfection of siRNAs targeting SULT2B1b, IL-6, TNF-α, NF-κB, IKKβ and IκB mRNA and protein expression were determined in Raw264.7 cells by real-time PCR and Western blot, respectively. The proliferative capacity was determined by EdU staining and Cell Counting Kit-8. Our data demonstrated that SULT2B1b knockdown could reduce phosphorylated NF-κB levels and downregulate IKKβ protein levels. Additionally, IκB levels were increased and the proliferation of ox-LDL stimulated cells was inhibited after SULT2B1b silencing. Downregulation of SULT2B1b expression was found to upregulate miR-148a-3p expression by microarray assay, while IKKβ was a miR-148a-3p target gene. Our study suggests that SULT2B1b knockdown could promote miR148a-3p expression and inhibit activation of the IKKβ/NF-κB signalling pathway, which suppressed the inflammatory response in macrophages. Therefore, targeting the SULT2B1b gene might be potentially beneficial for atherosclerosis prevention by decreasing the inflammatory response.