Nankai University

About: Nankai University is a education organization based out in Tianjin, China. It is known for research contribution in the topics: Catalysis & Enantioselective synthesis. The organization has 42964 authors who have published 51866 publications receiving 1127896 citations. The organization is also known as: Nánkāi Dàxué.

Mesoporous CuO–Fe2O3 composite catalysts for low-temperature carbon monoxide oxidation

Abstract: A series of mesoporous CuO–Fe 2 O 3 composite oxide catalysts with different CuO contents were prepared by a surfactant-assisted method of nanoparticle assembly. The prepared composite oxides were characterized by X-ray diffraction, N 2 adsorption, transmission electron microscopy, hydrogen temperature-programmed reduction, thermogravimetry–differential thermal analysis and X-ray photoelectron spectroscopy. Their catalytic behavior for low-temperature CO oxidation was studied by using a microreactor-GC system. These mesoporous CuO–Fe 2 O 3 catalysts possess a wormhole-like mesostructure with a narrow pore size distribution and high surface area, exhibiting high catalytic activity and stability for low-temperature CO oxidation. The catalytic behavior depended on the CuO content, the precalcination temperature, the surface area and the particle size of the catalysts. The catalyst with 15 mol% CuO content and calcined at 300 °C exhibited the highest catalytic activity and stability.

AMPK activation protects cells from oxidative stress-induced senescence via autophagic flux restoration and intracellular NAD(+) elevation.

Abstract: AMPK activation is beneficial for cellular homeostasis and senescence prevention. However, the molecular events involved in AMPK activation are not well defined. In this study, we addressed the mechanism underlying the protective effect of AMPK on oxidative stress-induced senescence. The results showed that AMPK was inactivated in senescent cells. However, pharmacological activation of AMPK by metformin and berberine significantly prevented the development of senescence and, accordingly, inhibition of AMPK by Compound C was accelerated. Importantly, AMPK activation prevented hydrogen peroxide-induced impairment of the autophagic flux in senescent cells, evidenced by the decreased p62 degradation, GFP-RFP-LC3 cancellation, and activity of lysosomal hydrolases. We also found that AMPK activation restored the NAD(+) levels in the senescent cells via a mechanism involving mostly the salvage pathway for NAD(+) synthesis. In addition, the mechanistic relationship of autophagic flux and NAD(+) synthesis and the involvement of mTOR and Sirt1 activities were assessed. In summary, our results suggest that AMPK prevents oxidative stress-induced senescence by improving autophagic flux and NAD(+) homeostasis. This study provides a new insight for exploring the mechanisms of aging, autophagy and NAD(+) homeostasis, and it is also valuable in the development of innovative strategies to combat aging.