Synthesis of disordered mesoporous silica loaded with ultrasmall-sized CuO nanoparticles based on an alkali-free strategy and its excellent catalytic performance in the reduction of organic dye.

In this paper, disordered mesoporous silica loaded with ultrasmall-sized and highly dispersed CuO nanoparticles was obtained by an alkali-free strategy. Pre-prepared copper bromoacetate (CuBA) and (3-aminopropyl)triethoxysilane (APTES) were selected as reactants, which can be covalently connected with each other for the formation of functional hybrid precursors. Simultaneously, the protonated amino group with the ability to promote the hydrolysis of silane was generated, avoiding any additional catalyst. The covalent introduction of copper salt by chemical bonding promised the molecular-level dispersion of copper ions, favouring the in situ generation of ultrasmall-sized and highly dispersed CuO nanoparticles in the silica matrix. The average diameter of this obtained composited silica material is around 700 nm, and CuO nanoparticles with an average diameter of ∼3 nm were uniformly dispersed in the silica matrix. Typically, disordered mesopores were obtained under the thermolysis of organic chains in the hybrid silica matrix; the BET surface area is 77 m2 g-1 and the pore diameter is about 2.5 nm. The catalytic property was investigated and the results show that this obtained CuO@mSiO2 material has good catalytic performance in the reduction of organic dye with NaBH4 as the reducing agent.

Alagebrium reduces glomerular fibrogenesis and inflammation beyond preventing RAGE activation in diabetic apolipoprotein E knockout mice.

Advanced glycation end products (AGEs) are important mediators of diabetic nephropathy that act through the receptor for AGEs (RAGE), as well as other mechanisms, to promote renal inflammation and glomerulosclerosis. The relative contribution of RAGE-dependent and RAGE-independent signaling pathways has not been previously studied in vivo. In this study, diabetic RAGE apoE double-knockout (KO) mice with streptozotocin-induced diabetes were treated with the AGE inhibitor, alagebrium (1 mg/kg/day), or the ACE inhibitor, quinapril (30 mg/kg/day), for 20 weeks, and renal parameters were assessed. RAGE deletion attenuated mesangial expansion, glomerular matrix accumulation, and renal oxidative stress associated with 20 weeks of diabetes. By contrast, inflammation and AGE accumulation associated with diabetes was not prevented. However, treatment with alagebrium in diabetic RAGE apoE KO mice reduced renal AGE levels and further reduced glomerular matrix accumulation. In addition, even in the absence of RAGE expression, alagebrium attenuated cortical inflammation, as denoted by the reduced expression of monocyte chemoattractant protein-1, intracellular adhesion molecule-1, and the macrophage marker cluster of differentiation molecule 11b. These novel findings confirm the presence of important RAGE-independent as well as RAGE-dependent signaling pathways that may be activated in the kidney by AGEs. This has important implications for the design of optimal therapeutic strategies for the prevention of diabetic nephropathy.