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1.
Front Chem ; 10: 1081319, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36583158

RESUMEN

Liquid organic hydrogen storage with N-ethylcarbazole (NEC) as a carrier is a very promising method. The use of precious metal hydrogenation catalysts restricts the development in industrial grade. Efficient and low-cost hydrogen storage catalysts are essential for its application. In this work, a Ni-Mo alloy catalyst supported by commercial activated carbon was synthesized by impregnation method, and the Ni-Mo ratio and preparation conditions were optimized. The catalyst was characterized by XRD, XPS, H2-TPR, SEM, and TEM. The results showed that the doping of Mo could dramatically promote the catalytic hydrogenation of N-ethylcarbazole by the Ni-based catalyst. More than 5.75 wt% hydrogenation could be achieved in 4 h using the Ni-Mo catalyst, and the selectivity of the fully hydrogenated product 12H-NEC could be effectively improved. This result reduces the cost of hydrogenation catalysts by more than 90% and makes liquid organic hydrogen storage a scaled possibility.

2.
Inorg Chem ; 58(17): 11793-11800, 2019 Sep 03.
Artículo en Inglés | MEDLINE | ID: mdl-31430123

RESUMEN

A series of silver coordination polymers (CPs) have been synthesized through self-assembly of three pyridinecarboxylic acid hydrazide (p-, m-, o-position) ligands with silver clusters (named Ag1-iah, Ag2-iah, and Ag3-iah). These silver CPs show different one- and two-dimensional topologies including cross-helical chains, planar network, and parallel helical chains for Ag1-iah, Ag2-iah, and Ag3-iah, respectively. The combination of experimental and computational results reveals the critical role in the space distribution of the coordination site of silver clusters and ligands in controlling the silver CPs' dimensionality and packing arrangement and modulating the optical properties and stability. Luminescent investigations reveal that Ag3-iah can selectively detect dichloromethane or trichloromethane in tetrachloromethane. These silver CPs provide a good model to study the influence of the space distribution of the coordination site of ligands on their packing arrangement and properties.

3.
Sci Rep ; 8(1): 4395, 2018 03 13.
Artículo en Inglés | MEDLINE | ID: mdl-29535398

RESUMEN

Reversal of activated hepatic stellate cells (HSCs) to a quiescent state and apoptosis of activated HSCs are key elements in the reversion of hepatic fibrosis. CCAAT/enhancer binding protein α (C/EBP-α) has been shown to inhibit HSC activation and promote its apoptosis. This study aims to investigate how C/EBP-α acetylation affects the fate of activated HSCs. Effects of a histone deacetylation inhibitor trichostatin A (TSA) on HSC activation were evaluated in a mouse model of liver fibrosis caused by carbon tetrachloride (CCl4) intoxication. TSA was found to ameliorate CCl4-induced hepatic fibrosis and improve liver function through increasing the protein level and enhancing C/EBP-α acetylation in the mouse liver. C/EBP-α acetylation was determined in HSC lines in the presence or absence of TSA, and the lysine residue K276 was identified as a main acetylation site in C/EBP-α protein. C/EBP-α acetylation increased its stability and protein level, and inhibited HSC activation. The present study demonstrated that C/EBP-α acetylation increases the protein level by inhibiting its ubiquitination-mediated degradation, and may be involved in the fate of activated HSCs. Use of TSA may confer an option in minimizing hepatic fibrosis by suppressing HSC activation, a key process in the initiation and progression of hepatic fibrosis.


Asunto(s)
Proteína alfa Potenciadora de Unión a CCAAT/metabolismo , Células Estrelladas Hepáticas/efectos de los fármacos , Células Estrelladas Hepáticas/metabolismo , Ácidos Hidroxámicos/farmacología , Acetilación , Animales , Apoptosis/efectos de los fármacos , Apoptosis/genética , Sitios de Unión , Biomarcadores , Proteína alfa Potenciadora de Unión a CCAAT/genética , Tetracloruro de Carbono/efectos adversos , Línea Celular , Expresión Génica , Células Estrelladas Hepáticas/patología , Humanos , Inmunohistoquímica , Cirrosis Hepática/etiología , Cirrosis Hepática/metabolismo , Cirrosis Hepática/patología , Masculino , Ratones , Mutación , Unión Proteica , Estabilidad Proteica , Ratas , Ubiquitinación
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