The enhanced antioxidant activity of surface-functionalized gold nanoparticles (AuNPs) synthesized by self-assembly has attracted great attention, but little is known about the mechanism behind the enhanced activity. To address this challenge, the antioxidant activity of Au@PEG3SA (i.e., surface-functionalization of spherical AuNPs with the antioxidant salvianic acid A) was used as an example to illustrate the mechanism of the enhanced activity. Evaluation of the antioxidant activity was performed in a radical-scavenging reaction between Au@PEG3SA and 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical. As expected, the rate constant for the reaction of Au@PEG3SA with DPPH was about nine times greater than that for the salvianic acid A monomer. A comparative analysis of the spectral characteristics of Au@PEG3SA and the salvianic acid A monomer further imply that the enhancement of the antioxidative reaction kinetics may be ascribed to the variation in the transition state for the DPPH-radical scavenging reaction through π-π stacking interactions between and among adjacent groups on the surface of Au@PEG3SA. On the other hand, the kinetic enhancement of Au@PEG3SA on reactive-oxygen-species (ROS) scavenging can be observed in living cells and in vivo, which possibly provides new insight for the bioapplication of self-assembly of surface-functionalized AuNPs.

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A metal–organic framework (SCNU-Z4) with high chemical stability in water and common organic solvents showed ability for iodine and dye adsorption.

Oxo-anion pollutants pose a serious threat to natural water systems. It is highly necessary to develop cationic porous materials capable of removing oxo-anion from sewage. However, they are relatively rarely reported compared with anionic and neutral materials. Herein, two cationic amorphous metal–organic cage-based solids containing cages of different sizes, namely, aMOC-1 and aMOC-2, were constructed and use for removing oxo-anions from water. Because the cages in these materials have large cavities (with about 3.5 and 4.5 nm in diameter for aMOC-1 and aMOC-2, respectively) and high positive charges (positive +24 for both), both aMOC-1 and aMOC-2 exhibit rapid kinetics in carcinogenic chromate (CrO4 2– and Cr2O7 2–) and ReO4 – (a surrogate anion of radioactive isotope TcO4 –) adsorption. The adsorption equilibrium can be reached within only a few minutes. The adsorption capacities of aMOC-1 for CrO4 2–, Cr2O7 2–, and ReO4 – are 157.4, 203.8, and 350 mg/g, respectively. Because aMOC-2 contains larger metal–organic cage, the corresponding adsorption capacities are 242.0, 407.0, and 583.9 mg/g, respectively. The capacity of aMOC-2 for Cr­(VI) oxo-anion adsorption ranks the highest among all related materials ever reported. In addition, the oxo-anions can be released rapidly within several minutes from the oxo-anion-loaded aMOCs in 2 M NaNO3 solution, which allows these materials to exhibit good reusability. Finally, the aMOCs have a potential application in the removal of Cr­(VI) from electroplating bath wastewater, in which the concentration changes from 10 to 0.17 ppm after treatment with aMOCs.

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The present study was designed to find out whether SB431542, an inhibitor of transforming growth factor beta1 activin receptor-like kinase, could protect the lung from LPS-induced injury. Inflammatory lung injury model was induced by intratracheal administration of LPS. C57BL/6 mice were randomly divided into the sham control group (S group), the LPS stimulation group (L group), the LPS + early SB431542 treatment group (Ie group), and the LPS + delayed SB431542 treatment group (Id group). SB431542 was admitted intraperitoneally on study days 1, 2, and 3 to the mice in Ie group, whereas those in Id group received the same dose of SB431542 on study days 4, 5, and 6. Pulmonary TNF-alpha and IL- 1beta mRNA expressions were tested. Pathological evaluations of pulmonary alveolitis and collagen deposition and fibrosis were performed on study days 7 and 28, along with the determination of pulmonary hydroxyproline, matrix metalloproteinase 9, and tissue inhibitor of matrix metalloproteinase 1 on study day 28. As a result, LPS stimulation resulted in significant increases of the pulmonary TNF-alpha and IL-1beta mRNA expressions as well as pathological scores for alveolitis on day 7 and increased collagen deposition, hydroxyproline content, and pathological scores for fibrosis on day 28, with a decrease of matrix metalloproteinase 9 activity. Those parameters were further aggravated in the Ie group whereas relieved significantly in the Id group. These data suggest that SB431542 therapy for inflammatory lung injury could be harmful if performed during early-phase inflammatory response. However, the therapy would prevent lung from inflammatory injury and fibrosis if it was initiated late.